Commensal bacterial antigen as a therapeutic agent for cancers

Abstract

The present disclosure relates to therapeutic compositions comprising commensal bacterial antigens and methods of use thereof.

Description

[0001] Docket No.103362-015WO1 COMMENSAL BACTERIAL ANTIGEN AS A THERAPEUTIC AGENT FOR CANCERS STATEMENT REGARDING FEDERALLY SPONSORED RESEARCH This invention was made with Government Support under Grant No.5U01AI125859 awarded by the National Institutes of Health. The Government has certain right in the invention. RELATED APPLICATION This PCT application claims priority to, and the benefit of, U.S. Provisional Patent Application No.63 / 667,297, filed July 3, 2024, entitled “COMMENSAL BACTERIAL ANTIGEN AS A THERAPEUTIC AGENT FOR CANCERS,” which is incorporated by reference herein in its entirety. REFERENCE TO SEQUENCE LISTING The sequence listing submitted on July 2, 2025, as an .XML file entitled “103362- 015WO1_ST26” created on July 2, 2025, and having a file size of 8,502 bytes is hereby incorporated by reference pursuant to 37 C.F.R. § 1.52(e)(5). FIELD The present disclosure relates to therapeutic compositions comprising commensal bacterial antigens and methods of use thereof. BACKGROUND Cancer immunotherapy has rapidly gained momentum in the last few years. Chimeric antigen receptor (CAR) T cells and antibodies targeting immune checkpoint molecules have been proven to be effective and prolong survival in a fraction of cancer patients. Investigation of checkpoint blockade responders and non-responders revealed that patients’ gut microbiome plays a significant role in the efficacy of such therapy. A previous study demonstrated that 11 commensal bacterial strains induce IFN- producing CD8+T cells in the intestine, and their mixture enhances the therapeutic efficacy of immune checkpoint inhibitors (ICI) in syngeneic tumor models. A more recent study reported that a microbiome signature generated from the MELRESIST study and three other melanoma studies might predict ICI response with 91% accuracy in melanoma and was also predictive of ICI response in non-small cell lung cancer (NSCLC), raising the question of whether bacterial antigens can be utilized for eliciting beneficial immune responses in the treatment of cancer. In contrast to the opportunistic pathogenic bacteria, the gastrointestinal tract harbors 1014 Docket No.103362-015WO1 commensal bacteria, collectively referred to as the microbiota. This intestinal commensal community, comprising thousands of nonpathogenic bacterial species, usually exists in peace with hosts. The microbiota is necessary for the development of the mucosal immune system. For instance, Segmented Filamentous Bacterium (SFB) elicits robust T helper 17 cells (Th17) responses in the small intestine, whereas type IV and XIVa Clostridia spp. potentiate regulatory T cell responses in the colon. SFB specifically induces Th17 that may be used for targeting certain tumors. However, the role of Th17 cells in tumor immunity and cancer immunotherapy is still not fully understood and controversial. There is a need to harness the power of commensal bacterial antigen-mediated Th17 cells for cancer immunotherapy. The compositions and methods disclosed herein address these and other needs. SUMMARY The present disclosure provides immunotherapeutic compositions comprising commensal bacterial antigens for treating and / or preventing cancer. The present disclosure also provides methods of using commensal bacterial antigens to treat and / or prevent cancer, to reduce and / or prevent tumor growth, and / or enhance the immune response of an immunotherapy. In some aspects, disclosed herein is an immunotherapeutic composition comprising a commensal bacterial antigen and a pharmaceutically acceptable carrier, wherein the commensal bacterial antigen comprises an epitope derived from a Segmented Filamentous Bacterium (SFB) (such as, for example a polypeptide expressed by the SFB including, but not limited to SFBNYU_003340 SFB polypeptide such as SEQ ID NO: 1). In some aspects, disclosed herein is a method of treating, reducing, decreasing, inhibiting, ameliorating, and / or preventing a cancer (such as, for example melanoma or lung cancer including, but not limited to metastatic cancers) in a subject in need thereof, the method comprising administering to the subject an immunotherapeutic composition of any preceding aspect. For example, disclosed herein is a method of treating a cancer in a subject in need thereof, the method comprising administering to the subject an immunotherapeutic composition comprising a commensal bacterial antigen and a pharmaceutically acceptable carrier, wherein the commensal bacterial antigen comprises an epitope derived from a Segmented Filamentous Bacterium (SFB) (such as, for example a polypeptide expressed by the SFB including, but not limited to SFBNYU_003340 SFB polypeptide such as SEQ ID NO: 1). In some aspects the immunotherapeutic composition is administered in combination with an immunotherapy including, but not limited to a chimeric antigen receptor (CAR), a monoclonal antibody, an immune checkpoint inhibitor (ICI), or a combination thereof. In some aspects, the method enhances an immune response to the immunotherapy. Docket No.103362-015WO1 In some aspects, disclosed herein is a method of preventing, inhibiting, decreasing, reducing, and / or preventing tumor growth (such as, for example, tumors of melanoma or lung cancer including, but not limited to metastatic tumors) in a subject in need thereof, the method comprising administering to the subject an immunotherapeutic composition of any preceding aspect. For example disclosed herein are is a method of preventing, inhibiting, decreasing, or reducing tumor growth in a subject in need thereof, the method comprising administering to the subject an immunotherapeutic composition comprising a commensal bacterial antigen and a pharmaceutically acceptable carrier, wherein the commensal bacterial antigen comprises an epitope derived from a Segmented Filamentous Bacterium (SFB) (such as, for example a polypeptide expressed by the SFB including, but not limited to SFBNYU_003340 SFB polypeptide such as SEQ ID NO: 1). In some aspects the immunotherapeutic composition is administered in combination with an immunotherapy including, but not limited to a chimeric antigen receptor (CAR), a monoclonal antibody, an immune checkpoint inhibitor (ICI), or a combination thereof. In some aspects, the method enhances an immune response to the immunotherapy. In some aspects, disclosed herein is a method of enhancing or increasing the efficacy of an immunotherapy in a subject, the method comprising administering to the subject an immunotherapeutic composition of any preceding aspect. For example, disclosed herein is a method of enhancing or increasing the efficacy of an immunotherapy in a subject, the method comprising administering to the subject an immunotherapeutic composition comprising a commensal bacterial antigen and a pharmaceutically acceptable carrier, wherein the commensal bacterial antigen comprises an epitope derived from a Segmented Filamentous Bacterium (SFB) (such as, for example a polypeptide expressed by the SFB including, but not limited to SFBNYU_003340 SFB polypeptide such as SEQ ID NO: 1). In some aspects the immunotherapeutic composition is administered in combination with an immunotherapy including, but not limited to a chimeric antigen receptor (CAR), a monoclonal antibody, an immune checkpoint inhibitor (ICI), or a combination thereof. In some aspects, the method enhances an immune response to the immunotherapy. In some embodiments, method of any preceding aspect reduces or prevents tumor growth. In some embodiments, the method of any preceding aspect increases one or more T cells, including, but not limited to CD4 T cells and CD8 T cells, in the subject. BRIEF DESCRIPTION OF FIGURES The accompanying figures, which are incorporated in and constitute a part of this specification, illustrate several aspects described below. Docket No.103362-015WO1 Figures 1A, 1B, and 1C show that that SFB drives Th17 expansion and coordinated immune reprogramming in intestinal and lung compartments (Figure 1A) Representative flow cytometry plots showing the frequency of SFB-specific Th17 cells (CD4+Vβ+) in the SILP (top) and lung (bottom) at weeks 0 (n=2), 1 (n=2), 2 (n=3), and 3 (n=3) post-SFB colonization. Numbers in each plot indicate the percentage of Vβ-expressing CD4+T cells within the live lymphocyte gate. Figure 1B shows the quantitative analysis of RORγt+CD4+T cell differentiation over time. Bar graphs show the mean percentage of specific T cell populations in the SILP (top) and Lung (bottom) at weeks 0 (n=2), 1 (n=2), 2 (n=3), and 3 (n=3) post-SFB colonization. Figure 1C shows the quantitative analysis of T- bet+CD4+and T-bet+CD8+T cell differentiation over time. Bar graphs show the mean percentage of specific T cell populations in the SILP (top) and Lung (bottom) at weeks 1, 2, and 3 post-SFB colonization. Figures 2A, 2B, 2C, and 2D show the expression of SFB epitope reduces metastatic burden and enhances Th17 infiltration in melanoma. Figure 2A shows the schematic workflow of experimental design. Mice were orally gavaged with SFB or PBS control, followed by intravenous injection of either B16F13340(expressing the SFB3340 Th17 epitope) or B16F1MEM(control) melanoma cells to establish a lung metastasis model. Figure 2B shows the representative macroscopic images of lung metastatic nodules demonstrating reduced tumor burden in SFB-colonized mice challenged with B16F13340compared to control conditions (left). Quantitative analysis of lung tumor burden shown as mean number of nodules per lung (± SEM) across experimental groups (n=5 mice per group) *p<0.05, **p<0.01, ***p<0.001 (unpaired Student's t-test) (right). Figure 2C shows the representative flow cytometry plots revealing enhanced IL17A responses alongside increased effector cytokine production, IFN-γ, and TNF-α in CD4+TILs isolated from lung metastases. Numbers indicate the percentage of cells in each quadrant. Figure 2D show the quantification of IL17A+, IFN- γ+, and TNF-α+populations among CD4+TILs (mean% ± SEM. *p<0.05, **p<0.01, ***p<0.001(unpaired Student's t-test). Figures 3A, 3B, 3C, 3D, and 3E show that the SFB antigen increases tumor immunogenicity and enhances anti-tumor immune responses. Figure 3A shows the representative flow cytometry plots showing IFN-γ+, TNF-α+, and IL-17A+populations among CD8+TILs isolated from lung metastases across all four experimental groups (SFB+ / B16F1SFB3340, SFB+ / B16F1MEM, SFB- / B16F1SFB3340, SFB- / B16F1MEM). Numbers indicate the percentage of positive cells in each gate. Figure 3B shows the quantitative analysis of effector cytokine-producing CD8+T cells within lung metastases. Bar graphs show a mean percentage (± SEM) of IFN-γ+, IL-17A+, and TNF-α+among CD8+TILs for each experimental group. *p<0.05, **p<0.01, ***p<0.001(unpaired Student's t-test). Figure 3C shows the representative flow cytometry plots and quantitative analysis of NK cells (CD3-NK1.1+). Figure 3D Docket No.103362-015WO1 shows the representative flow cytometry plots gated with NK1.1+and quantitative analysis of IFN-γ+NK cells in lung metastases across experimental groups. *p<0.05, **p<0.01, ***p<0.001(unpaired Student's t-test). Figure 3E shows the representative flow cytometry plots showing the frequency of Gr-1hi, Gr-1int, and CD11c in lung metastases across all four experimental groups (left). Right: Quantification of Gr-1hi, Gr-1int, CD11c+as percentage of total CD45+cells, with notable trends observed in the SFB+ / B16F1SFB3340 group (right). (mean% ± SEM. *p<0.05, **p<0.01, ***p<0.001(unpaired Student's t-test). Figure 4 shows that the SFB antigen bridges gut-tumor immunity. Correlation analysis between immune cell cytokine production and lung tumor burden across different experimental groups. Scatter plots depict the relationship between the percentage of cytokine-producing immune cells and the number of lung tumor nodules in mice inoculated with SFB-B16F1MEM(green, n=5), SFB-B16F13340(blue, n=5), and SFB+B16F13340(orange, n=4). Left panels: CD4+T cell cytokine production showing IFN-γ+cells (top) and TNF-α+cells (bottom). Middle / right panels: CD8+T cell cytokine production displaying IFN-γ+cells (top), TNF-α+cells (bottom), and IL-17A+cells (bottom). Right panel: IFN-γ+NK cells (top). Pearson correlation coefficients (r) quantify the linear association between variables for each experimental group, with values ranging from -1 (perfect negative correlation) to +1 (perfect positive correlation). Each data point represents an individual mouse, and trend lines indicate the direction and strength of correlation within each treatment group. Figures 5A, 5B, 5C, 5D, and 5E show the SFB-driven systemic metabolic reprogramming enhances anti-tumor immunity. Figure 5A shows the schematic representation of metabolite sample collection strategy from Naïve, SFB-positive (SFB+), B16F13340, SFB+B16F13340, and SFB+B16F1MEMmice across serum, bronchoalveolar lavage fluid (BALF), and feces. (n=7 mice per group). Figure 5B shows the principal component analysis (PCA) score plot showing metabolomics clustering of sample groups based on component 1 (PC1) versus component 2 (PC2), demonstrating distinct metabolic profiles between experimental conditions. Figure 5C shows the quantitative comparison of differential metabolites between SFB- and SFB+B16F13340 tumor-bearing mice across three biological compartments (serum, BALF, and feces), showing the number of significantly altered metabolites in each sample type. Figure 5D shows the metabolite category composition analysis displaying the distribution of upregulated and downregulated metabolites by functional class between SFB- and SFB+B16F13340 tumor-bearing mice across three biological compartments (serum, BALF, and feces). Figure 5E shows the heat map visualization of the top 10 upregulated metabolites in B16F13340tumor- bearing mice across all three sample types (serum, BALF, and feces), accompanied by individual pie charts showing the upregulated metabolic pathway composition for each biological compartment. Docket No.103362-015WO1 DETAILED DESCRIPTION The following description of the disclosure is provided as an enabling teaching of the disclosure in its best, currently known embodiment(s). To this end, those skilled in the relevant art will recognize and appreciate that many changes can be made to the various embodiments of the invention described herein, while still obtaining the beneficial results of the present disclosure. It will also be apparent that some of the desired benefits of the present disclosure can be obtained by selecting some of the features of the present disclosure without utilizing other features. Accordingly, those who work in the art will recognize that many modifications and adaptations to the present disclosure are possible and can even be desirable in certain circumstances and are a part of the present disclosure. Thus, the following description is provided as illustrative of the principles of the present disclosure and not in limitation thereof. Reference will now be made in detail to the embodiments of the invention, examples of which are illustrated in the drawings and the examples. This invention may, however, be embodied in many different forms and should not be construed as limited to the embodiments set forth herein. Terminology Unless defined otherwise, all technical and scientific terms used herein have the same meaning as commonly understood to one of ordinary skill in the art to which this disclosure belongs. The term “comprising” and variations thereof as used herein is used synonymously with the term “including” and variations thereof and are open, non-limiting terms. Although the terms “comprising” and “including” have been used herein to describe various embodiments, the terms “consisting essentially of” and “consisting of” can be used in place of “comprising” and “including” to provide for more specific embodiments and are also disclosed. As used in this disclosure and in the appended claims, the singular forms “a”, “an”, “the”, include plural referents unless the context clearly dictates otherwise. The following definitions are provided for the full understanding of terms used in this specification. The terms "about" and "approximately" are defined as being “close to” as understood by one of ordinary skill in the art. In one non-limiting embodiment the terms are defined to be within 10%. In another non-limiting embodiment, the terms are defined to be within 5%. In still another non- limiting embodiment, the terms are defined to be within 1%. Ranges can be expressed herein as from “about” one particular value, and / or to “about” another particular value. When such a range is expressed, another embodiment includes from the one particular value and / or to the other particular value. Similarly, when values are expressed as Docket No.103362-015WO1 approximations, by use of the antecedent “about,” it will be understood that the particular value forms another embodiment. It will be further understood that the endpoints of each of the ranges are significant both in relation to the other endpoint, and independently of the other endpoint. It is also understood that there are a number of values disclosed herein, and that each value is also herein disclosed as “about” that particular value in addition to the value itself. For example, if the value “10” is disclosed, then “about 10” is also disclosed. It is also understood that when a value is disclosed that “less than or equal to” the value, “greater than or equal to the value” and possible ranges between values are also disclosed, as appropriately understood by the skilled artisan. For example, if the value “10” is disclosed the “less than or equal to 10”as well as “greater than or equal to 10” is also disclosed. It is also understood that the throughout the application, data is provided in a number of different formats, and that this data, represents endpoints and starting points, and ranges for any combination of the data points. For example, if a particular data point “10” and a particular data point 15 are disclosed, it is understood that greater than, greater than or equal to, less than, less than or equal to, and equal to 10 and 15 are considered disclosed as well as between 10 and 15. It is also understood that each unit between two particular units are also disclosed. For example, if 10 and 15 are disclosed, then 11, 12, 13, and 14 are also disclosed. “Optional” or “optionally” means that the subsequently described event or circumstance may or may not occur, and that the description includes instances where said event or circumstance occurs and instances where it does not. An "increase" can refer to any change that results in a greater amount of a symptom, disease, composition, condition, or activity. An increase can be any individual, median, or average increase in a condition, symptom, activity, composition in a statistically significant amount. Thus, the increase can be a 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 15, 20, 25, 30, 35, 40, 45, 50, 55, 60, 65, 70, 75, 80, 85, 90, 95, 100% or more increase so long as the increase is statistically significant. A "decrease" can refer to any change that results in a smaller amount of a symptom, disease, composition, condition, or activity. A substance is also understood to decrease the genetic output of a gene when the genetic output of the gene product with the substance is less relative to the output of the gene product without the substance. Also, for example, a decrease can be a change in the symptoms of a disorder such that the symptoms are less than previously observed. A decrease can be any individual, median, or average decrease in a condition, symptom, activity, composition in a statistically significant amount. Thus, the decrease can be a 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 15, 20, 25, 30, 35, 40, 45, 50, 55, 60, 65, 70, 75, 80, 85, 90, 95, 100%, or more decrease so long as the decrease is statistically significant. Docket No.103362-015WO1 The terms “treat,” “treating,” and grammatical variations thereof as used herein, include partially or completely delaying, alleviating, mitigating or reducing the intensity of one or more attendant symptoms of a disorder or condition and / or alleviating, mitigating or impeding one or more causes of a disorder or condition. Treatments according to the disclosure may be applied preventively, prophylactically, palliatively or remedially. Treatments are administered to a subject prior to onset (e.g., before obvious signs of disease, such as a cancer), during early onset (e.g., upon initial signs and symptoms of disease, such as a cancer), or after an established development of a disease, such as a cancer. "Inhibit," "inhibiting," and "inhibition" mean to decrease an activity, response, condition, disease, or other biological parameter. This can include but is not limited to the complete ablation of the activity, response, condition, or disease. This may also include, for example, a 10% reduction in the activity, response, condition, or disease as compared to the native or control level. Thus, the reduction can be a 10, 20, 30, 40, 50, 60, 70, 80, 90, 100%, or any amount of reduction below, above, or in between the given ranges as compared to native or control levels. By “reduce” or other forms of the word, such as “reducing” or “reduction,” means lowering of an event or characteristic (e.g., tumor growth). It is understood that this is typically in relation to some standard or expected value, in other words it is relative, but that it is not always necessary for the standard or relative value to be referred to. For example, “reduces tumor growth” means reducing the rate of growth of a tumor relative to a standard or a control. By “prevent” or other forms of the word, such as “preventing” or “prevention,” is meant to stop a particular event or characteristic, to stabilize or delay the development or progression of a particular event or characteristic, or to minimize the chances that a particular event or characteristic will occur. Prevent does not require comparison to a control as it is typically more absolute than, for example, reduce. As used herein, something could be reduced but not prevented, but something that is reduced could also be prevented. Likewise, something could be prevented but not reduced, but something that is prevented could also be reduced. It is understood that where reduce or prevent are used, unless specifically indicated otherwise, the use of the other word is also expressly disclosed. The term “subject” refers to any individual who is the target of administration or treatment. The subject can be a vertebrate, for example, a mammal. In one aspect, the subject can be human, non-human primate, bovine, equine, porcine, canine, or feline. The subject can also be a guinea pig, rat, hamster, rabbit, mouse, or mole. Thus, the subject can be a human or veterinary patient. The term “patient” refers to a subject under the treatment of a clinician, e.g., physician. Docket No.103362-015WO1 The term “therapeutically effective amount” refers to the amount of the composition used is of sufficient quantity to ameliorate one or more causes or symptoms of a disease or disorder. Such amelioration only requires a reduction or alteration, not necessarily elimination. The term “treatment” refers to the medical management of a patient with the intent to cure, ameliorate, stabilize, or prevent a disease, pathological condition, or disorder. This term includes active treatment, that is, treatment directed specifically toward the improvement of a disease, pathological condition, or disorder, and also includes causal treatment, that is, treatment directed toward removal of the cause of the associated disease, pathological condition, or disorder. In addition, this term includes palliative treatment, that is, treatment designed for the relief of symptoms rather than the curing of the disease, pathological condition, or disorder; preventative treatment, that is, treatment directed to minimizing or partially or completely inhibiting the development of the associated disease, pathological condition, or disorder; and supportive treatment, that is, treatment employed to supplement another specific therapy directed toward the improvement of the associated disease, pathological condition, or disorder. "Comprising" is intended to mean that the compositions, methods, etc. include the recited elements, but do not exclude others. "Consisting essentially of'' when used to define compositions and methods, shall mean including the recited elements, but excluding other elements of any essential significance to the combination. Thus, a composition consisting essentially of the elements as defined herein would not exclude trace contaminants from the isolation and purification method and pharmaceutically acceptable carriers, such as phosphate buffered saline, preservatives, and the like. "Consisting of'' shall mean excluding more than trace elements of other ingredients and substantial method steps for administering the compositions provided and / or claimed in this disclosure. Embodiments defined by each of these transition terms are within the scope of this disclosure. “Composition” refers to any agent that has a beneficial biological effect. Beneficial biological effects include both therapeutic effects, e.g., treatment of a disorder or other undesirable physiological condition, and prophylactic effects, e.g., prevention of a disorder or other undesirable physiological condition. The terms also encompass pharmaceutically acceptable, pharmacologically active derivatives of beneficial agents specifically mentioned herein, including, but not limited to, a vector, polynucleotide, cells, salts, esters, amides, proagents, active metabolites, isomers, fragments, analogs, and the like. When the term “composition” is used, then, or when a particular composition is specifically identified, it is to be understood that the term includes the composition per se as well as pharmaceutically acceptable, pharmacologically active vector, polynucleotide, salts, esters, amides, proagents, conjugates, active metabolites, isomers, fragments, analogs, etc. “Expression” as used herein refers to the process by which information from a gene is used in Docket No.103362-015WO1 the synthesis of a functional gene product that enables it to produce a peptide / protein end product, and ultimately affect a phenotype, as the final effect. Reference also is made herein to peptides, polypeptides, proteins, and compositions comprising peptides, polypeptides, and proteins. As used herein, a polypeptide and / or protein is defined as a polymer of amino acids, typically of length≥100 amino acids (Garrett & Grisham, Biochemistry, 2nd edition, 1999, Brooks / Cole, 110). A peptide is defined as a short polymer of amino acids, of a length typically of 20 or less amino acids, and more typically of a length of 12 or less amino acids (Garrett & Grisham, Biochemistry, 2nd edition, 1999, Brooks / Cole, 110). The peptides, polypeptides, and proteins disclosed herein may be modified to include non- amino acid moieties. Modifications may include but are not limited to carboxylation (e.g., N-terminal carboxylation via addition of a di-carboxylic acid having 4-7 straight-chain or branched carbon atoms, such as glutaric acid, succinic acid, adipic acid, and 4,4-dimethylglutaric acid), amidation (e.g., C- terminal amidation via addition of an amide or substituted amide such as alkylamide or dialkylamide), PEGylation (e.g., N-terminal or C-terminal PEGylation via additional of polyethylene glycol), acylation (e.g., O-acylation (esters), N-acylation (amides), S-acylation (thioesters)), acetylation (e.g., the addition of an acetyl group, either at the N-terminus of the protein or at lysine residues), formylation lipoylation (e.g., attachment of a lipoate, a C8 functional group), myristoylation (e.g., attachment of myristate, a C14 saturated acid), palmitoylation (e.g., attachment of palmitate, a C16 saturated acid), alkylation (e.g., the addition of an alkyl group, such as an methyl at a lysine or arginine residue), isoprenylation or prenylation (e.g., the addition of an isoprenoid group such as farnesol or geranylgeraniol), amidation at C-terminus, glycosylation (e.g., the addition of a glycosyl group to either asparagine, hydroxylysine, serine, or threonine, resulting in a glycoprotein). Distinct from glycation, which is regarded as a nonenzymatic attachment of sugars, polysialylation (e.g., the addition of polysialic acid), glypiation (e.g., glycosylphosphatidylinositol (GPI) anchor formation, hydroxylation, iodination (e.g., of thyroid hormones), and phosphorylation (e.g., the addition of a phosphate group, usually to serine, tyrosine, threonine, or histidine). The phrases “percent identity” and “% identity,” as applied to polypeptide sequences, refer to the percentage of residue matches between at least two polypeptide sequences aligned using a standardized algorithm. Methods of polypeptide sequence alignment are well-known. Some alignment methods consider conservative amino acid substitutions. Such conservative substitutions, explained in more detail above, generally preserve the charge and hydrophobicity at the site of substitution, thus preserving the structure (and therefore function) of the polypeptide. Percent identity for amino acid sequences may be determined as understood in the art. (See, e.g., U.S. Pat. No. 7,396,664, which is incorporated herein by reference in its entirety). A suite of commonly used and Docket No.103362-015WO1 freely available sequence comparison algorithms is provided by the National Center for Biotechnology Information (NCBI) Basic Local Alignment Search Tool (BLAST) (Altschul, S. F. et al. (1990) J. Mol. Biol.215:403410), which is available from several sources, including the NCBI, Bethesda, Md., at its website. The BLAST software suite includes various sequence analysis programs including “blastp,” that is used to align a known amino acid sequence with other amino acids sequences from a variety of databases. Percent identity may be measured over the length of an entire defined polypeptide sequence or may be measured over a shorter length, for example, over the length of a fragment taken from a larger, defined polypeptide sequence, for instance, a fragment of at least 15, at least 20, at least 30, at least 40, at least 50, at least 70 or at least 150 contiguous residues. Such lengths are exemplary only, and it is understood that any fragment length may be used to describe a length over which percentage identity may be measured. The term “variant” means a polypeptide derived from a parent polypeptide by one or more (several) alteration(s), i.e., a substitution, insertion, and / or deletion, at one or more (several) positions. A substitution means a replacement of an amino acid occupying a position with a different amino acid; a deletion means removal of an amino acid occupying a position; and an insertion means adding 1 or more, such as 1, 2, 3, 4, 5, 6, 7, 8, 9 or 10, preferably 1-3 amino acids immediately adjacent an amino acid occupying a position. In relation to substitutions, ‘immediately adjacent’ may be to the N-side (‘upstream’) or C-side (‘downstream’) of the amino acid occupying a position (‘the named amino acid’). Therefore, for an amino acid named / numbered ‘X,’ the insertion may be at position ‘X+1’ (‘downstream’) or at position ‘X−1’ (‘upstream’). A “variant” of a particular polypeptide sequence may be defined as a polypeptide sequence having at least 50% sequence identity to the particular polypeptide sequence over a certain length of one of the polypeptide sequences using blastp with the “BLAST 2 Sequences” tool available at the National Center for Biotechnology Information's website. (See Tatiana A. Tatusova, Thomas L. Madden (1999), “Blast 2 sequences—a new tool for comparing protein and nucleotide sequences”, FEMS Microbiol Lett. 174:247-250). In some embodiments a variant polypeptide may show, for example, at least 60%, at least 70%, at least 80%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99% or greater sequence identity over a certain defined length relative to a reference polypeptide. A variant polypeptide may have substantially the same functional activity as a reference polypeptide. For example, a variant polypeptide may exhibit or more biological activities associated with binding a ligand and / or binding DNA at a specific binding site. Variants comprising a fragment of a reference amino acid sequence are contemplated herein. Docket No.103362-015WO1 A “fragment” is a portion of an amino acid sequence which is identical in sequence to but shorter in length than the reference sequence. A fragment may comprise up to the entire length of the reference sequence, minus at least one amino acid residue. For example, a fragment may comprise from 5 to 1000 contiguous amino acid residues of a reference polypeptide, respectively. In some embodiments, a fragment may comprise at least 5, 10, 15, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 40, 50, 60, 70, 80, 90, 100, 150, 250, or 500 contiguous amino acid residues of a reference polypeptide, respectively. Fragments may be preferentially selected from certain regions of a molecule, for example the N- terminal region and / or the C-terminal region of a polypeptide. The term “at least a fragment” encompasses the full length polypeptide. The term “administer,” “administering”, or derivatives thereof refer to delivering a composition, substance, inhibitor, or medication to a subject or object by one or more the following routes: oral, topical, intravenous, subcutaneous, transcutaneous, transdermal, intramuscular, intra- joint, parenteral, intra-arteriole, intradermal, intraventricular, intracranial, intraperitoneal, intralesional, intranasal, rectal, vaginal, by inhalation or via an implanted reservoir. The term “parenteral” includes subcutaneous, intravenous, intramuscular, intra-articular, intra-synovial, intrasternal, intrathecal, intrahepatic, intralesional, and intracranial injections or infusion techniques. The terms “immunotherapy” and “immunotherapeutic” refers to the treatment of disease by activating or suppressing the immune system. In cancer treatment, the most effective immunotherapies are cell- based immunotherapies that utilize lymphocytes, macrophages, dendritic cells, natural killer cells, cytotoxic T lymphocytes, etc. to defend the body against cancer by targeting abnormal antigens expressed on the surface of tumor cells. The term “cancer” is used to address any neoplastic disease, and is not limited to epithelial neoplasms (surface and glandular cancers; such a squamous cancers or adenomas)). It is used here to describe both solid tumors and hematologic malignancies, including but not limited to epithelial (surface and glandular) cancers, soft tissue and bone sarcomas, angiomas, mesothelioma, melanoma, lymphomas, leukemias and myeloma. A “pharmaceutically effective amount” of a drug necessary to achieve a therapeutic effect may vary according to factors such as the age, sex, and weight of the subject. Dosage regimens can be adjusted to provide the optimum therapeutic response. For example, several divided doses may be administered daily, or the dose may be proportionally reduced as indicated by the exigencies of the therapeutic situation. "Pharmaceutically acceptable carrier" (sometimes referred to as a “carrier”) means a carrier or excipient that is useful in preparing a pharmaceutical or therapeutic composition that is generally safe and non-toxic and includes a carrier that is acceptable for veterinary and / or human Docket No.103362-015WO1 pharmaceutical or therapeutic use. The terms "carrier" or "pharmaceutically acceptable carrier" can include, but are not limited to, phosphate buffered saline solution, water, emulsions (such as an oil / water or water / oil emulsion) and / or various types of wetting agents. An “epitope” or “antigenic determinant” refer to the part of an antigen, a molecular structure, or foreign particulate that can bind to a specific antibody or T-cell receptor. The presence of antigens or epitopes of antigens within a host can illicit an immune response. An “antigen” refers to a molecule, moiety, foreign particulate matter, or an allergen that can bind to a specific antibody or T cell receptor. The presence of antigens within a host can illicit an immune response against said molecule, moiety, foreign particulate matter, or allergen. Cancer Therapeutic Compositions Advances in cancer immunotherapy are increasing the potential for improving treatments of cancer. However, many cancers remain unresponsive to certain immunotherapies. For example, some patients with melanoma or non-small cell lung cancer (NSCLC) have primary resistance to immune- checkpoint inhibitors (ICIs) alone despite these tumor types being among the most responsive to such agents. Thus, there is a need for more effective treatment approaches to address the issue of resistance. The human microbiota has important implications for tumorigenesis and cancer therapy. Studies into the existence and pathological relevance of microbiota in cancer have revealed that such bacteria are not mere bystanders in the microenvironment, but they actively contribute to cancer dynamics, including tumor inhibition and modulating the immune environment. Notably, the presence of microbiota in tumors are implicated as having unique anti-cancer properties that distinguish them from conventional anticancer agents. In has also been found that some microbiota species can selectively target cancerous tissues, penetrate deep into tumors, undergo exponential growth and remodel the immune microenvironment. Thus, the present disclosure provides therapeutic compositions and methods of use thereof comprising a peptide and / or epitope derived from a Segmented Filamentous Bacterium (SFB), or fragment thereof. The present disclosure provides immunotherapeutic compositions comprising commensal bacterial antigens for treating and / or preventing cancer. The present disclosure also provides methods of using commensal bacterial antigens to treat and / or prevent cancer, to reduce and / or prevent tumor growth, and / or enhance the immune response of an immunotherapy. In some aspects, disclosed herein is an immunotherapeutic composition comprising a commensal bacterial antigen and a pharmaceutically acceptable carrier, wherein the commensal bacterial antigen comprises an epitope derived from a Segmented Filamentous Bacterium (SFB). Segmented Filamentous Bacterium (SFB) are members of the mammalian gut microbiota shown to Docket No.103362-015WO1 potently induce an immune response. SFB are gram-positive, spore forming, filamentous bacteria ranging from about 0.7 to 1.8 µm in diameter and as long as 80 µm in length. SFB has also been identified as a pivotal member of the commensal microbiota affecting the ontogeny and function of the host immune system. In some embodiments, the “pharmaceutically acceptable" component can refer to a component that is not biologically or otherwise undesirable, i.e., the component may be incorporated into a pharmaceutical formulation of the invention and administered to a subject as described herein without causing significant undesirable biological effects or interacting in a deleterious manner with any of the other components of the formulation in which it is contained. When used in reference to administration to a human, the term generally implies the component has met the required standards of toxicological and manufacturing testing or that it is included on the Inactive Ingredient Guide prepared by the U.S. Food and Drug Administration. "Pharmaceutically acceptable carrier" (sometimes referred to as a “carrier”) means a carrier or excipient that is useful in preparing a pharmaceutical or therapeutic composition that is generally safe and non-toxic, and includes a carrier that is acceptable for veterinary and / or human pharmaceutical or therapeutic use. The terms "carrier" or "pharmaceutically acceptable carrier" can include, but are not limited to, phosphate buffered saline solution, water, emulsions (such as an oil / water or water / oil emulsion) and / or various types of wetting agents. As used herein, the term “carrier” encompasses any excipient, diluent, filler, salt, buffer, stabilizer, solubilizer, lipid, stabilizer, or other material well known in the art for use in pharmaceutical formulations. The choice of a carrier for use in a composition will depend upon the intended route of administration for the composition. The preparation of pharmaceutically acceptable carriers and formulations containing these materials is described in, e.g., Remington's Pharmaceutical Sciences, 21st Edition, ed. University of the Sciences in Philadelphia, Lippincott, Williams & Wilkins, Philadelphia, PA, 2005. Examples of physiologically acceptable carriers include saline, glycerol, DMSO, buffers such as phosphate buffers, citrate buffer, and buffers with other organic acids; antioxidants including ascorbic acid; low molecular weight (less than about 10 residues) polypeptides; proteins, such as serum albumin, gelatin, or immunoglobulins; hydrophilic polymers such as polyvinylpyrrolidone; amino acids such as glycine, glutamine, asparagine, arginine or lysine; monosaccharides, disaccharides, and other carbohydrates including glucose, mannose, or dextrins; chelating agents such as EDTA; sugar alcohols such as mannitol or sorbitol; salt-forming counterions such as sodium; and / or nonionic surfactants such as TWEENTM(ICI, Inc.; Bridgewater, New Jersey), polyethylene glycol (PEG), and PLURONICSTM(BASF; Florham Park, NJ). To provide for the administration of such dosages for the desired therapeutic treatment, compositions disclosed herein Docket No.103362-015WO1 can advantageously comprise between about 0.1% and 99% by weight of the total of one or more of the subject compounds based on the weight of the total composition including carrier or diluent. In some embodiments, the epitope of any preceding aspect comprises a polypeptide expressed by the SFB, including but not limited to a SFBNYU_003340 SFB polypeptide. In some embodiments, the epitope of any preceding aspect comprises SEQ ID NO: 1, or a fragment thereof. In some embodiments, the epitope of any preceding aspect comprises 80%, 85%, 90%, 95%, 98%, 99%, or 100% sequence identity to SEQ ID NO: 1. In some embodiments, the epitope of any preceding aspect comprises SEQ ID NO: 6, or a fragment thereof. In some embodiments, the epitope of any preceding aspect comprises 70%, 75%, 80%, 85%, 90%, 95%, 98%, 99%, or 100% sequence identity to SEQ ID NO: 6. In some embodiments, the immunotherapeutic composition of any preceding aspect is administered in combination with an immunotherapy. In some embodiments, the immunotherapy includes, but is not limited to an immune checkpoint inhibitor, a monoclonal antibody, a chimeric antigen receptor, cytokines, or a combination thereof. In some embodiments, the immunotherapy includes, but is not limited to interferons, cytokines (e.g., tumor necrosis factor, interferon α, interferon γ), vaccines, hematopoietic growth factors, monoclonal serotherapy, immunostimulants and / or immunodulatory agents (e.g., IL-1, 2, 4, 6, or 12), immune cell growth factors (e.g., GM-CSF) and antibodies (e.g. HERCEPTIN (trastuzumab), T-DM1, AVASTIN (bevacizumab), ERBITUX (cetuximab), VECTIBIX (panitumumab), RITUXAN (rituximab), BEXXAR (tositumomab)), anti- estrogens (e.g. tamoxifen, raloxifene, and megestrol), LHRH agonists (e.g. goscrclin and leuprolide), anti-androgens (e.g. flutamide and bicalutamide), photodynamic therapies (e.g. vertoporfin (BPD- MA), phthalocyanine, photosensitizer Pc4, and demethoxy-hypocrellin A (2BA-2-DMHA)), nitrogen mustards (e.g. cyclophosphamide, ifosfamide, trofosfamide, chlorambucil, estramustine, and melphalan), nitrosoureas (e.g. carmustine (BCNU) and lomustine (CCNU)), alkylsulphonates (e.g. busulfan and treosulfan), triazenes (e.g. dacarbazine, temozolomide), platinum containing compounds (e.g. cisplatin, carboplatin, oxaliplatin), vinca alkaloids (e.g. vincristine, vinblastine, vindesine, and vinorelbine), taxoids (e.g. paclitaxel or a paclitaxel equivalent such as nanoparticle albumin-bound paclitaxel (ABRAXANE), docosahexaenoic acid bound-paclitaxel (DHA-paclitaxel, Taxoprexin), polyglutamate bound-paclitaxel (PG-paclitaxel, paclitaxel poliglumex, CT-2103, XYOTAX), the tumor-activated prodrug (TAP) ANG1005 (Angiopep-2 bound to three molecules of paclitaxel), paclitaxel-EC-1 (paclitaxel bound to the erbB2-recognizing peptide EC-1), and glucose- conjugated paclitaxel, e.g., 2′-paclitaxel methyl 2-glucopyranosyl succinate; docetaxel, taxol), epipodophyllins (e.g. etoposide, etoposide phosphate, teniposide, topotecan, 9-aminocamptothecin, camptoirinotecan, irinotecan, crisnatol, mytomycin C), anti-metabolites, DHFR inhibitors (e.g. Docket No.103362-015WO1 methotrexate, dichloromethotrexate, trimetrexate, edatrexate), IMP dehydrogenase inhibitors (e.g. mycophenolic acid, tiazofurin, ribavirin, and EICAR), ribonucleotide reductase inhibitors (e.g. hydroxyurea and deferoxamine), uracil analogs (e.g.5-fluorouracil (5-FU), floxuridine, doxifluridine, ratitrexed, tegafur-uracil, capecitabine), cytosine analogs (e.g. cytarabine (ara C), cytosine arabinoside, and fludarabine), purine analogs (e.g. mercaptopurine and Thioguanine), Vitamin D3 analogs (e.g. EB 1089, CB 1093, and KH 1060), isoprenylation inhibitors (e.g. lovastatin), dopaminergic neurotoxins (e.g. 1-methyl-4-phenylpyridinium ion), cell cycle inhibitors (e.g. staurosporine), actinomycin (e.g. actinomycin D, dactinomycin), bleomycin (e.g. bleomycin A2, bleomycin B2, peplomycin), anthracycline (e.g. daunorubicin, doxorubicin, pegylated liposomal doxorubicin, idarubicin, epirubicin, pirarubicin, zorubicin, mitoxantrone), MDR inhibitors (e.g. verapamil), Ca2+ATPase inhibitors (e.g. thapsigargin), imatinib, thalidomide, lenalidomide, tyrosine kinase inhibitors (e.g., axitinib (AG013736), bosutinib (SKI-606), cediranib (RECENTIN™, AZD2171), dasatinib (SPRYCEL®, BMS-354825), erlotinib (TARCEVA®), gefitinib (IRESSA®), imatinib (Gleevec®, CGP57148B, STI-571), lapatinib (TYKERB®, TYVERB®), lestaurtinib (CEP- 701), neratinib (HKI-272), nilotinib (TASIGNA®), semaxanib (semaxinib, SU5416), sunitinib (SUTENT®, SU11248), toceranib (PALLADIA®), vandetanib (ZACTIMA®, ZD6474), vatalanib (PTK787, PTK / ZK), trastuzumab (HERCEPTIN®), bevacizumab (AVASTIN®), rituximab (RITUXAN®), cetuximab (ERBITUX®), panitumumab (VECTIBIX®), ranibizumab (Lucentis®), nilotinib (TASIGNA®), sorafenib (NEXAVAR®), everolimus (AFINITOR®), alemtuzumab (CAMPATH®), gemtuzumab ozogamicin (MYLOTARG®), temsirolimus (TORISEL®), ENMD- 2076, PCI-32765, AC220, dovitinib lactate (TKI258, CHIR-258), BIBW 2992 (TOVOK™), SGX523, PF-04217903, PF-02341066, PF-299804, BMS-777607, ABT-869, MP470, BIBF 1120 (VARGATEF®), AP24534, JNJ-26483327, MGCD265, DCC-2036, BMS-690154, CEP-11981, tivozanib (AV-951), OSI-930, MM-121, XL-184, XL-647, and / or XL228), proteasome inhibitors (e.g., bortezomib (VELCADE)), mTOR inhibitors (e.g., rapamycin, temsirolimus (CCI-779), everolimus (RAD-001), ridaforolimus, AP23573 (Ariad), AZD8055 (AstraZeneca), BEZ235 (Novartis), BGT226 (Norvartis), XL765 (Sanofi Aventis), PF-4691502 (Pfizer), GDC0980 (Genetech), SF1126 (Semafoe) and OSI-027 (OSI)), oblimersen, gemcitabine, caminomycin, leucovorin, pemetrexed, cyclophosphamide, dacarbazine, procarbizine, prednisolone, dexamethasone, campathecin, plicamycin, asparaginase, aminopterin, methopterin, porfiromycin, melphalan, leurosidine, leurosine, chlorambucil, trabectedin, procarbazine, discodermolide, caminomycin, aminopterin, and hexamethyl melamine. Methods of Use Docket No.103362-015WO1 In some aspects, disclosed herein is a method of treating a cancer in a subject in need thereof, the method comprising administering to the subject an immunotherapeutic composition comprising a commensal bacterial antigen and a pharmaceutically acceptable carrier, wherein the commensal bacterial antigen comprises an epitope derived from a Segmented Filamentous Bacterium (SFB). In some aspects, disclosed herein is a method of preventing or reducing tumor growth in a subject in need thereof, the method comprising administering to the subject an immunotherapeutic composition comprising a commensal bacterial antigen and a pharmaceutically acceptable carrier, wherein the commensal bacterial antigen comprises an epitope derived from a Segmented Filamentous Bacterium (SFB). In some aspects, disclosed herein is a method of enhancing an immunotherapy in a subject, the method comprising administering to the subject an immunotherapeutic composition comprising a commensal bacterial antigen and a pharmaceutically acceptable carrier, wherein the commensal bacterial antigen comprises an epitope derived from a Segmented Filamentous Bacterium (SFB). In some embodiments, the method of any preceding aspect comprises an epitope comprising a polypeptide expressed by the SFB including but not limited to a SFBNYU_003340 SFB polypeptide. In some embodiments, the method of any preceding aspect comprises an epitope comprising SEQ ID NO: 1, or a fragment thereof. In some embodiments, the method of any preceding aspect comprises an epitope comprising 80%, 85%, 90%, 95%, 98%, 99%, or 100% sequence identity to SEQ ID NO: 1. In some embodiments, the method of any preceding aspect comprises an epitope comprising SEQ ID NO: 6, or a fragment thereof. In some embodiments, the method of any preceding aspect comprises an epitope comprising 70%, 75%, 80%, 85%, 90%, 95%, 98%, 99%, or 100% sequence identity to SEQ ID NO: 6. In some embodiments, the method of any preceding aspect comprises an immunotherapeutic composition being administered in combination with an immunotherapy. In some embodiments, the immunotherapy includes, but is not limited to interferons, cytokines (e.g., tumor necrosis factor, interferon α, interferon γ), vaccines, hematopoietic growth factors, monoclonal serotherapy, immunostimulants and / or immunodulatory agents (e.g., IL-1, 2, 4, 6, or 12), immune cell growth factors (e.g., GM-CSF) and antibodies (e.g. HERCEPTIN (trastuzumab), T-DM1, AVASTIN (bevacizumab), ERBITUX (cetuximab), VECTIBIX (panitumumab), RITUXAN (rituximab), BEXXAR (tositumomab)), anti-estrogens (e.g. tamoxifen, raloxifene, and megestrol), LHRH agonists (e.g. goscrclin and leuprolide), anti-androgens (e.g. flutamide and bicalutamide), photodynamic therapies (e.g. vertoporfin (BPD-MA), phthalocyanine, photosensitizer Pc4, and demethoxy-hypocrellin A (2BA-2-DMHA)), nitrogen mustards (e.g. cyclophosphamide, ifosfamide, Docket No.103362-015WO1 trofosfamide, chlorambucil, estramustine, and melphalan), nitrosoureas (e.g. carmustine (BCNU) and lomustine (CCNU)), alkylsulphonates (e.g. busulfan and treosulfan), triazenes (e.g. dacarbazine, temozolomide), platinum containing compounds (e.g. cisplatin, carboplatin, oxaliplatin), vinca alkaloids (e.g. vincristine, vinblastine, vindesine, and vinorelbine), taxoids (e.g. paclitaxel or a paclitaxel equivalent such as nanoparticle albumin-bound paclitaxel (ABRAXANE), docosahexaenoic acid bound-paclitaxel (DHA-paclitaxel, Taxoprexin), polyglutamate bound- paclitaxel (PG-paclitaxel, paclitaxel poliglumex, CT-2103, XYOTAX), the tumor-activated prodrug (TAP) ANG1005 (Angiopep-2 bound to three molecules of paclitaxel), paclitaxel-EC-1 (paclitaxel bound to the erbB2-recognizing peptide EC-1), and glucose-conjugated paclitaxel, e.g., 2′-paclitaxel methyl 2-glucopyranosyl succinate; docetaxel, taxol), epipodophyllins (e.g. etoposide, etoposide phosphate, teniposide, topotecan, 9-aminocamptothecin, camptoirinotecan, irinotecan, crisnatol, mytomycin C), anti-metabolites, DHFR inhibitors (e.g. methotrexate, dichloromethotrexate, trimetrexate, edatrexate), IMP dehydrogenase inhibitors (e.g. mycophenolic acid, tiazofurin, ribavirin, and EICAR), ribonucleotide reductase inhibitors (e.g. hydroxyurea and deferoxamine), uracil analogs (e.g. 5-fluorouracil (5-FU), floxuridine, doxifluridine, ratitrexed, tegafur-uracil, capecitabine), cytosine analogs (e.g. cytarabine (ara C), cytosine arabinoside, and fludarabine), purine analogs (e.g. mercaptopurine and Thioguanine), Vitamin D3 analogs (e.g. EB 1089, CB 1093, and KH 1060), isoprenylation inhibitors (e.g. lovastatin), dopaminergic neurotoxins (e.g. 1-methyl-4- phenylpyridinium ion), cell cycle inhibitors (e.g. staurosporine), actinomycin (e.g. actinomycin D, dactinomycin), bleomycin (e.g. bleomycin A2, bleomycin B2, peplomycin), anthracycline (e.g. daunorubicin, doxorubicin, pegylated liposomal doxorubicin, idarubicin, epirubicin, pirarubicin, zorubicin, mitoxantrone), MDR inhibitors (e.g. verapamil), Ca2+ATPase inhibitors (e.g. thapsigargin), imatinib, thalidomide, lenalidomide, tyrosine kinase inhibitors (e.g., axitinib (AG013736), bosutinib (SKI-606), cediranib (RECENTIN™, AZD2171), dasatinib (SPRYCEL®, BMS-354825), erlotinib (TARCEVA®), gefitinib (IRESSA®), imatinib (Gleevec®, CGP57148B, STI-571), lapatinib (TYKERB®, TYVERB®), lestaurtinib (CEP-701), neratinib (HKI-272), nilotinib (TASIGNA®), semaxanib (semaxinib, SU5416), sunitinib (SUTENT®, SU11248), toceranib (PALLADIA®), vandetanib (ZACTIMA®, ZD6474), vatalanib (PTK787, PTK / ZK), trastuzumab (HERCEPTIN®), bevacizumab (AVASTIN®), rituximab (RITUXAN®), cetuximab (ERBITUX®), panitumumab (VECTIBIX®), ranibizumab (Lucentis®), nilotinib (TASIGNA®), sorafenib (NEXAVAR®), everolimus (AFINITOR®), alemtuzumab (CAMPATH®), gemtuzumab ozogamicin (MYLOTARG®), temsirolimus (TORISEL®), ENMD-2076, PCI-32765, AC220, dovitinib lactate (TKI258, CHIR-258), BIBW 2992 (TOVOK™), SGX523, PF-04217903, PF- 02341066, PF-299804, BMS-777607, ABT-869, MP470, BIBF 1120 (VARGATEF®), AP24534, Docket No.103362-015WO1 JNJ-26483327, MGCD265, DCC-2036, BMS-690154, CEP-11981, tivozanib (AV-951), OSI-930, MM-121, XL-184, XL-647, and / or XL228), proteasome inhibitors (e.g., bortezomib (VELCADE)), mTOR inhibitors (e.g., rapamycin, temsirolimus (CCI-779), everolimus (RAD-001), ridaforolimus, AP23573 (Ariad), AZD8055 (AstraZeneca), BEZ235 (Novartis), BGT226 (Norvartis), XL765 (Sanofi Aventis), PF-4691502 (Pfizer), GDC0980 (Genetech), SF1126 (Semafoe) and OSI-027 (OSI)), oblimersen, gemcitabine, caminomycin, leucovorin, pemetrexed, cyclophosphamide, dacarbazine, procarbizine, prednisolone, dexamethasone, campathecin, plicamycin, asparaginase, aminopterin, methopterin, porfiromycin, melphalan, leurosidine, leurosine, chlorambucil, trabectedin, procarbazine, discodermolide, caminomycin, aminopterin, and hexamethyl melamine. In some embodiments, the method of any preceding aspect treats or prevents a cancer including, but not limited to acoustic neuroma, adenocarcinoma, adrenal gland cancer, anal cancer, angiosarcoma (e.g., lymphangiosarcoma, lymphangioendotheliosarcoma, hemangiosarcoma), appendix cancer, benign monoclonal gammopathy, biliary cancer (e.g., cholangiocarcinoma), bladder cancer, breast cancer (e.g., adenocarcinoma of the breast, papillary carcinoma of the breast, mammary cancer, medullary carcinoma of the breast), brain cancer (e.g., meningioma; glioma, e.g., astrocytoma, oligodendroglioma; medulloblastoma), bronchus cancer, carcinoid tumor, cervical cancer (e.g., cervical adenocarcinoma), choriocarcinoma, chordoma, craniopharyngioma, colorectal cancer (e.g., colon cancer, rectal cancer, colorectal adenocarcinoma), epithelial carcinoma, ependymoma, endotheliosarcoma (e.g., Kaposi's sarcoma, multiple idiopathic hemorrhagic sarcoma), endometrial cancer (e.g., uterine cancer, uterine sarcoma), esophageal cancer (e.g., adenocarcinoma of the esophagus, Barrett's adenocarinoma), Ewing's sarcoma, eye cancer (e.g., intraocular melanoma, retinoblastoma), familiar hypereosinophilia, gall bladder cancer, gastric cancer (e.g., stomach adenocarcinoma), gastrointestinal stromal tumor (GIST), head and neck cancer (e.g., head and neck squamous cell carcinoma, oral cancer (e.g., oral squamous cell carcinoma (OSCC), throat cancer (e.g., laryngeal cancer, pharyngeal cancer, nasopharyngeal cancer, oropharyngeal cancer)), hematopoietic cancers (e.g., leukemia such as acute lymphocytic leukemia (ALL) (e.g., B-cell ALL, T-cell ALL), acute myelocytic leukemia (AML) (e.g., B-cell AML, T-cell AML), chronic myelocytic leukemia (CML) (e.g., B-cell CML, T-cell CML), and chronic lymphocytic leukemia (CLL) (e.g., B-cell CLL, T-cell CLL); lymphoma such as Hodgkin lymphoma (HL) (e.g., B-cell HL, T-cell HL) and non- Hodgkin lymphoma (NHL) (e.g., B-cell NHL such as diffuse large cell lymphoma (DLCL) (e.g., diffuse large B-cell lymphoma (DLBCL)), follicular lymphoma, chronic lymphocytic leukemia / small lymphocytic lymphoma (CLL / SLL), mantle cell lymphoma (MCL), marginal zone B-cell lymphomas (e.g., mucosa-associated lymphoid tissue (MALT) lymphomas, nodal marginal zone B-cell lymphoma, splenic marginal zone B-cell lymphoma), primary mediastinal B-cell lymphoma, Burkitt Docket No.103362-015WO1 lymphoma, lymphoplasmacytic lymphoma (i.e., “Waldenstrom's macroglobulinemia”), hairy cell leukemia (HCL), immunoblastic large cell lymphoma, precursor B-lymphoblastic lymphoma and primary central nervous system (CNS) lymphoma; and T-cell NHL such as precursor T-lymphoblastic lymphoma / leukemia, peripheral T-cell lymphoma (PTCL) (e.g., cutaneous T-cell lymphoma (CTCL) (e.g., mycosis fungiodes, Sezary syndrome), angioimmunoblastic T-cell lymphoma, extranodal natural killer T-cell lymphoma, enteropathy type T-cell lymphoma, subcutaneous panniculitis-like T- cell lymphoma, anaplastic large cell lymphoma); a mixture of one or more leukemia / lymphoma as described above; and multiple myeloma (MM)), heavy chain disease (e.g., alpha chain disease, gamma chain disease, mu chain disease), hemangioblastoma, inflammatory myofibroblastic tumors, immunocytic amyloidosis, kidney cancer (e.g., nephroblastoma a.k.a. Wilms' tumor, renal cell carcinoma), liver cancer (e.g., hepatocellular cancer (HCC), malignant hepatoma), lung cancer (e.g., bronchogenic carcinoma, small cell lung cancer (SCLC), non-small cell lung cancer (NSCLC), adenocarcinoma of the lung), leiomyosarcoma (LMS), mastocytosis (e.g., systemic mastocytosis), myelodysplastic syndrome (MDS), mesothelioma, myeloproliferative disorder (MPD) (e.g., polycythemia Vera (PV), essential thrombocytosis (ET), agnogenic myeloid metaplasia (AMM) a.k.a. myelofibrosis (MF), chronic idiopathic myelofibrosis, chronic myelocytic leukemia (CML), chronic neutrophilic leukemia (CNL), hypereosinophilic syndrome (HES)), neuroblastoma, neurofibroma (e.g., neurofibromatosis (NF) type 1 or type 2, schwannomatosis), neuroendocrine cancer (e.g., gastroenteropancreatic neuroendoctrine tumor (GEP-NET), carcinoid tumor), osteosarcoma, ovarian cancer (e.g., cystadenocarcinoma, ovarian embryonal carcinoma, ovarian adenocarcinoma), papillary adenocarcinoma, pancreatic cancer (e.g., pancreatic adenocarcinoma, intraductal papillary mucinous neoplasm (IPMN), Islet cell tumors), penile cancer (e.g., Paget's disease of the penis and scrotum), pinealoma, primitive neuroectodermal tumor (PNT), prostate cancer (e.g., prostate adenocarcinoma), rectal cancer, rhabdomyosarcoma, salivary gland cancer, skin cancer (e.g., squamous cell carcinoma (SCC), keratoacanthoma (KA), melanoma, basal cell carcinoma (BCC)), small bowel cancer (e.g., appendix cancer), soft tissue sarcoma (e.g., malignant fibrous histiocytoma (MFH), liposarcoma, malignant peripheral nerve sheath tumor (MPNST), chondrosarcoma, fibrosarcoma, myxosarcoma), sebaceous gland carcinoma, sweat gland carcinoma, synovioma, testicular cancer (e.g., seminoma, testicular embryonal carcinoma), thyroid cancer (e.g., papillary carcinoma of the thyroid, papillary thyroid carcinoma (PTC), medullary thyroid cancer), urethral cancer, vaginal cancer and vulvar cancer (e.g., Paget's disease of the vulva). The therapeutic composition of any preceding aspect may be administered in such amounts, time, and route deemed necessary in order to achieve the desired result. The exact amount of the therapeutic composition of any preceding aspect will vary from subject to subject, depending on the Docket No.103362-015WO1 species, age, and general condition of the subject, the severity of the cancer, the particular therapeutic composition of any preceding aspect, its mode of administration, its mode of activity, and the like. The therapeutic composition of any preceding aspect is preferably formulated in dosage unit form for ease of administration and uniformity of dosage. It will be understood, however, that the total daily usage of the therapeutic composition of any preceding aspect will be decided by the attending physician within the scope of sound medical judgment. The specific therapeutically effective dose level for any particular subject will depend upon a variety of factors including the cancer being treated and the severity of the cancer; the activity of the therapeutic composition of any preceding aspect employed; the specific therapeutic composition of any preceding aspect employed; the age, body weight, general health, sex and diet of the patient; the time of administration, route of administration, and rate of excretion of the specific therapeutic composition of any preceding aspect employed; the duration of the treatment; drugs used in combination or coincidental with the specific therapeutic composition of any preceding aspect employed; and like factors well known in the medical arts. The therapeutic composition of any preceding aspect may be administered by any route. In some embodiments, the therapeutic composition of any preceding aspect is administered via a variety of routes, including oral, intravenous, intramuscular, intra-arterial, intramedullary, intrathecal, subcutaneous, intraventricular, transdermal, interdermal, rectal, intravaginal, intraperitoneal, topical (as by powders, ointments, creams, and / or drops), mucosal, nasal, buccal, enteral, sublingual; by intratracheal instillation, bronchial instillation, and / or inhalation; and / or as an oral spray, nasal spray, and / or aerosol. In general, the most appropriate route of administration will depend upon a variety of factors including the nature of the therapeutic composition of any preceding aspect (e.g., its stability in the environment of the gastrointestinal tract), the condition of the subject (e.g., whether the subject is able to tolerate oral administration), etc. The exact amount of therapeutic composition of any preceding aspect required to achieve a therapeutically effective amount will vary from subject to subject, depending on species, age, and general condition of a subject, severity of the side effects, identity of the particular compound(s), mode of administration, and the like. The amount to be administered to, for example, a child or an adolescent can be determined by a medical practitioner or person skilled in the art and can be lower or the same as that administered to an adult. In some embodiments, the therapeutic composition of any preceding aspect is administered 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49, 50, 51, 52, 53, 54, 55, 56, 57, 58, 59, 60, 61, 62, 63, 64, 65, 66, 67, 68, 69, 70, 71, 72, 73, 74, 75, 76, 77, 78, 79, 80, 81, 82, 83, 84, 85, 86, 87, 88, 89, 90, 91, 92, 93, 94, 95, 96, 97, 98, 99, 100, or more times. In some embodiments, Docket No.103362-015WO1 the therapeutic composition of any preceding aspect is administered daily. In some embodiments, the therapeutic composition of any preceding aspect is administered every day, every 2 days, every 3 days, every 4 days, every 5 days, every 6 days, every 7 days, or more. In some embodiments, the therapeutic composition of any preceding aspect is administered every week, every 2 weeks, every 3 weeks, every 4 weeks, or more. In some embodiments, the therapeutic composition of any preceding aspect is administered every month, every 2 months, every 3 months, every 4 months, every 5 months, every 6 months, every 7 months, every 8 months, every 9 months, every 10 months, every 11 months, every 12 months, or more. In some embodiments, the therapeutic composition of any preceding aspect is administered every year, every 2 years, every 3 years, every 4 years, every 5 years, or more. In some embodiments, the method of any preceding aspect enhances an immune response to the immunotherapy. In some embodiments, the method of any preceding aspect enhances an immune response to the immunotherapeutic composition by 10%, 15%, %, 25%, 30%, 35%, 45%, 50%, 55%, 60%, 65%, 70%, 75%, 80%, 85%, 90%, 95%, 99%, 100%, or more relative to a control immunotherapeutic composition. In some embodiments, the method of any preceding aspect reduces or prevents tumor growth. In some embodiments, the method of any preceding aspect reduces or prevents tumor growth by 10%, 15%, %, 25%, 30%, 35%, 45%, 50%, 55%, 60%, 65%, 70%, 75%, 80%, 85%, 90%, 95%, 99%, 100%, or more relative to a control immunotherapeutic composition. In some embodiments, the method of any preceding aspect increases one or more T cells, including, but not limited to CD4 T cells and CD8 T cells, in the subject. In some embodiments, the method of any preceding aspect increases one or more T cells of any preceding aspect by 10%, 15%, %, 25%, 30%, 35%, 45%, 50%, 55%, 60%, 65%, 70%, 75%, 80%, 85%, 90%, 95%, 99%, 100%, or more relative to a control immunotherapeutic composition. A number of embodiments of the disclosure have been described. Nevertheless, it will be understood that various modifications may be made without departing from the spirit and scope of the invention. Accordingly, other embodiments are within the scope of the following claims. By way of non-limiting illustration, examples of certain embodiments of the present disclosure are given below. EXAMPLES The following examples are set forth below to illustrate the compositions, devices, methods, and results according to the disclosed subject matter. These examples are not intended to be inclusive of all aspects of the subject matter disclosed herein, but rather to illustrate representative methods and Docket No.103362-015WO1 results. These examples are not intended to exclude equivalents and variations of the present invention which are apparent to one skilled in the art. EXAMPLE 1: COMMENSAL BACTERIAL ANTIGEN AS A THERAPEUTIC AGENT FOR CANCERS A previous study discovered that a TCR that is enriched in Th17 cells (called 7B8 TCR) succeeded in mapping an I-Ab-restricted epitope, which is derived from SFBNYU_003340 (referred to as 3340), Segmented Filamentous Bacterium (SFB) unique protein. To determine the role of bacterial antigen- mediated Th17 cells in anti-tumor immunity, we generated a B16-SFB3340 melanoma cell line that expressed an SFB epitope to facilitate Th17 cell recruitment into the tumors. We injected B16-3340 or B16-MEM (Mock control) tumor cells intravenously to grow tumors in the lung in SFB- and SFB+mice. We found that lung tumor nodules were significantly decreased in B16-3340 tumor-bearing SFB- mice compared with B16-MEM control tumor-bearing mice. SFB colonization further decreased tumor growth in B16-3340 tumor-bearing mice. In addition, Th17, Th1, and CD8+IFNγ+cells were increased in the lungs of the B16-3340 tumor-bearing mice compared with B16-MEM control tumor-bearing mice, and tumor control positively correlated with CD4+Th17 cells and other T effectors, which indicated that SFB- specific Th17 cells enhance immune effector response in lung metastatic B16 melanoma in an antigen- dependent manner. EXAMPLE 2: COMMENSAL BACTERIAL ANTIGEN-MEDIATED IMMUNE RESPONSE ENHANCES ANTI- TUMOR IMMUNITY Cancer immunotherapy has revolutionized treatment paradigms but remains limited by substantial heterogeneity in clinical outcomes, while T helper 17 (Th17) cells exhibit context- dependent roles in cancer. Segmented filamentous bacteria (SFB) represent prototypical commensals capable of inducing intestinal Th17 cells with systemic effects. The present disclosure elucidates how SFB antigen-mediated immune responses modulate the tumor microenvironment and manifest anti- tumor efficacy through a coordinated gut-lung immunological axis. Using a lentivirus system, the SFB epitope SFB3340 and a control vector was genetically expressed in B16F1 melanoma cells and it was investigated whether the SFB antigen modulates tumor immunogenicity. SFB3340-expressing B16F1 cells (B16-3340) and control vector-expressing B16F1 cells (B16-MEM) were intravenously injected to grow tumors in the lung in SFB- and SFB+C57BL / 6 mice. Subsequently, tumor growth was examined in the lung and immune cell populations were characterized in the tumor microenvironment using flow cytometry. In addition, comprehensive untargeted metabolomics analysis was performed to investigate whether SFB antigens modulate immune response through alterations in metabolic homeostasis. Docket No.103362-015WO1 Lung tumor nodules were significantly decreased in B16-3340 tumor-bearing SFB-negative mice compared with B16-MEM control tumor-bearing mice. SFB colonization further reduced tumor growth in B16-3340 tumor-bearing mice. Th1, Th17, and CD8+IFNγ+T cells were all increased in the lungs of the B16-3340 tumor-bearing mice compared with B16-MEM control tumor-bearing mice, and tumor control positively correlated with CD4+Th17 cells, other T effectors, and activated NK cells. Metabolomics data demonstrated the coordinated upregulation of microbial-derived metabolites, including hippurate, 3-phenylpropionate, and p-cresol derivatives, across multiple tissue compartments. The expression of SFB antigen within tumors enhances anti-tumor immunity through comprehensive immune microenvironment remodeling and metabolic reprogramming via a gut-lung axis mechanism that bridges innate microbial recognition with adaptive anti-tumor immunity. The present disclosure offers significant translational potential for developing microbiome-leveraged cancer immunotherapies that overcome current treatment limitations. Cancer immunotherapy has revolutionized treatment paradigms across multiple malignancies, demonstrating unprecedented durable responses in previously intractable cancers. However, this success has been tempered by substantial heterogeneity in clinical outcomes, with response rates varying dramatically between cancer types and even among patients with the same malignancy. This variability underscores the critical need to unravel the multifaceted determinants of therapeutic efficacy to expand the benefits of immunotherapy to a broader patient population. T helper 17 (Th17) cells have emerged as critical mediators of mucosal immunity, with complex and seemingly contradictory roles in cancer progression. In some cancers, Th17 responses promote tumor growth through angiogenesis and immunosuppression, while in others, they enhance anti-tumor immunity through cytotoxic T cell recruitment and natural killer cell activation. While Th17 cells demonstrate complex roles in cancer progression, emerging evidence reveals their potential to benefit the immune checkpoint blockade treatment outcome, with Th17-inducing dendritic cell vaccines successfully overcoming ICB resistance in ovarian cancer, higher IL-17A frequencies correlating with melanoma patient responses to anti-PD-1 therapy, and Th17-enhancing strategies converting immunologically cold tumors into responsive targets for checkpoint inhibition. The molecular and contextual determinants underlying these divergent functions remain poorly understood, presenting a significant challenge in harnessing Th17 biology for therapeutic benefit. Segmented filamentous bacteria (SFB) represent a prototypical commensal capable of potently inducing intestinal Th17 cells through epithelial attachment and antigen-specific stimulation. SFB-induced Th17 cells possess unique transcriptional and functional properties that distinguish them from pathogen-driven Th17 responses, exhibiting enhanced mucosal protective functions while Docket No.103362-015WO1 maintaining immunological homeostasis. Importantly, SFB-induced Th17 cells exert systemic effects beyond the gut, migrating to peripheral organs, including the lungs, through established gut-lung axis communication pathways. The combination of this systemic reach and their antigen-specific recognition capabilities positions SFB-induced Th17 cells as promising candidates for therapeutic redirection toward anti-tumor immunity. However, whether this microbiome-primed Th17 immunity can be therapeutically redirected against cancer cells, particularly through epitope engineering strategies that might enhance immunotherapy efficacy, remains unexplored and represents a critical knowledge gap at the intersection of microbiome immunology and cancer immunotherapy. Here, the mechanistic basis by which SFB-mediated Th17 immune responses orchestrate comprehensive remodeling of the tumor microenvironment and manifest potent anti-tumor efficacy through a coordinated gut-lung immunological axis. These findings demonstrate that SFB epitope presentation within the metastatic niche robustly activates tumor-infiltrating Th17 cells, which subsequently orchestrate a multifaceted anti-tumor cytokine cascade characterized by enhanced production of IL-17A and IFN-γ across diverse immune effector populations, including CD4+T cells, CD8+T cells, and activation of cytotoxic natural killer cells. This epitope-driven immune activation establishes a synergistic relationship between commensal bacterial immunity and anti-tumor surveillance, effectively bridging innate microbial recognition pathways with adaptive anti-cancer responses. Furthermore, the comprehensive metabolomics profiling identifies coordinated alterations in aromatic amino acid metabolism and microbial-derived compounds across multiple tissue compartments, showing that SFB-mediated metabolic reprogramming creates a systemic biochemical environment that potentiates anti-tumor immunity. This integrated approach offers significant translational possibilities for developing next-generation cancer immunotherapies that leverage the natural immunomodulatory capacity of the host microbiome to overcome current limitations in cancer treatment efficacy. METHODS Mice C57BL / 6J mice were purchased from The Jackson Laboratory (Bar Harbor, ME, USA) and maintained according to the established guidelines. All animal procedures were conducted in accordance with protocols approved by the Institutional Animal Care and Use Committee (IACUC) at The Ohio State University and adhered to the National Institutes of Health Guide for the Care and Use of Laboratory Animals. Mice were routinely monitored for the presence of SFB through fecal screening. SFB-positive C57BL / 6 mice obtained from Taconic Biosciences (Rensselaer, NY, USA). Docket No.103362-015WO1 Reagents Antibodies used for flow cytometry were obtained from BD Biosciences (Mountain View, CA), eBioscience (San Diego, CA), BioLegend (San Diego, CA), TONBO biosciences (San Diego, CA), and Thermo Fisher Scientific (Waltham, MA) (Table 1). All other chemicals were obtained from Sigma-Aldrich and Fisher Scientific. SFB screening by quantitative qPCR A fecal pellet was crushed in 2 ml of PBS and filtered through a 40-μm cell strainer. The FastPrep-24™ Classic bead beating grinder and lysis system (MP Biomedicals) was used for sample homogenization with 0.1mm zirconia / silica beads at a speed of 6.5 for 1 min. Bacterial DNA was isolated from the cell lysate supernatant after spinning down at 15000 rpm for 1 min and purified with the DNA Clean& Concentrator Kit (Zymo Research). Quantitative PCR was performed using SsoAdvanced Universal SYBR Green supermix (Bio-Rad) with published sequences conducted in triplicate (SFB736F, 5’-GACACTGAGGCATGAGAGCAT(SEQ ID NO: 2)-3’; SFB844R, 5’- GACGGCACGGATTGTTATTCA(SEQ ID NO: 3)-3’; UnitF340, 5’- ACTCCTACGGGAGGCAGCAGT(SEQ ID NO: 4)-3’; UnitR514, 5’- ATTACCGCGGCTGCTGGC(SEQ ID NO: 5)-3’). The Cq (quantification cycle) value of the qPCR results of SFB-specific 16S rRNA was normalized by the Cq value of eubacteria 16S rRNA. Isolation of lymphocyte For isolation of tissue-resident lymphocytes, spleens were mechanically disrupted and filtered through a 100-μm cell strainer (BD Biosciences, cat#352360), followed by erythrocyte lysis using ACK buffer (155mM NH4Cl, 10mM KCHO3, 0.127mM EDTA). For lung lymphocyte isolation, mice were perfused with 10 mL perfusion solution (0.15mg / ml heparin) via the right ventricle prior to tissue harvest. Lung tissue was minced into 1-2 mm fragments and incubated in 40 mL of 1.3 mM EDTA solution at 37°C for 30 minutes with gentle agitation. After centrifugation (300 × g, 5 minutes), tissue fragments were suspended in 40 mL RPMI 1640 digestion buffer containing 5% FBS, 1 mM MgCl₂, 1 mM CaCl₂, and 0.4 mg / mL Collagenase D (Roche, cat#11088866001) and incubated at 37°C for an hour with intermittent agitation. The enzymatic reaction was terminated by the addition of 40 mL of cold complete RPMI 1640 medium. The digested tissue was further dissociated by gentle mechanical disruption and filtered through 100-μm cell strainers (BD Biosciences, cat#352360). Lymphocytes were enriched by density gradient centrifugation using 44% / 67% Percoll gradients (Cytiva, cat#17089101) at 800 × g for 20 minutes at room temperature with brake disengaged. Cells Docket No.103362-015WO1 at the interface were carefully collected, washed twice with PBS containing 2% FBS, and used for subsequent flow cytometric analysis. Flow cytometry For intracellular cytokine analysis, single cell suspensions were stimulated with phorbol 12- myristate 13-acetate (PMA, 50 ng / mL, Sigma-Aldrich, cat#P8139), ionomycin (500 ng / mL, Sigma- Aldrich, cat#I0634), and brefeldin A (BFA, 10 μg / mL, Invitrogen, #00-4506-51) in complete T cell medium (RPMI 1640 supplemented with 10% FBS, 2 mM L-glutamine, 1% penicillin / streptomycin, and 55 μM β-mercaptoethanol) at 37°C in a humidified atmosphere with 5% CO₂ for 2 hours. Following restimulation, cells were incubated with anti-CD16 / CD32 antibodies (1:200, Biolegend cat#101320) to block FcγRII / III receptors for 10 minutes at 4°C and subsequently stained with fluorochrome-conjugated surface antibodies for 30 minutes at 4°C. After washing twice with FACS buffer (PBS with 2% FBS), cells were resuspended in 7-AAD viability staining solution (Invitrogen, cat#00-6993-50) to exclude dead cells. For intracellular staining, cells viability was stained with Ghost Dye Fixable Viability Dye prior to surface staining and subsequently fixed and permeabilized using the Foxp3 / Transcription Factor Staining Buffer Set (eBioscience, Thermo Fisher Scientific) according to the manufacturer's protocol and stained with the appropriate antibodies. Data were acquired on a Cytek Aurora spectral flow cytometer and analyzed using FlowJo software V10 (BD Biosciences). Cell culture B16F1-MEM (vector control) and B16F1-3340 (SFB epitope engineered) murine melanoma cells (derived from B16F1, ATCC CRL-6323, authenticated by morphological assessment and melanin production) were maintained in Dulbecco's Modified Eagle's Medium (DMEM, Gibco, cat#D5796-500ml) supplemented with 10% heat-inactivated fetal bovine serum (Gibco Fetal Bovine Serum, cat#26140087), 100 U / mL penicillin / streptomycin (Gibco, cat#15140-122100ml) at 37°C in a humidified atmosphere with 5% CO2. Cells were cultured in T-75 flasks (Falcon, cat#353136) and passaged at 80-90% confluence using 0.25% trypsin-EDTA (Gibco, cat#25200056), followed by centrifugation at 300 × g for 5 minutes. Stable transfectants were maintained under selection with 5ug / ml puromycin (Sigma, cat#P9620-10mL), which was removed from the culture medium 24 hours before in vivo experiments. For tumor rejection studies, cells were harvested, washed twice with sterile PBS (Cellpro, cat#PB500), and resuspended at 2 × 10⁶ cells / mL in PBS. Cell viability was assessed immediately before implantation using Trypan Blue exclusion (Sigma, cat#T8154-100ml), Docket No.103362-015WO1 with all preparations maintaining >95% viability. Mice received 2 × 10⁵ viable cells / 100 μL via tail vein injection. Metabolon sample preparation and analysis Serum collection was performed following anesthesia, and cardiac puncture was performed using a 22-gauge needle to collect blood samples directly from the heart. Blood samples were immediately placed on ice for 30 minutes to allow coagulation, then centrifuged at 13,000 rpm for 20 minutes at 4°C to separate serum. The resulting serum samples were flash-frozen in liquid nitrogen and stored at -80°C until further analysis. Bronchoalveolar Lavage Fluid (BALF) Collection: The trachea was surgically exposed by carefully removing the overlying skin and fascia. A sterile catheter was inserted into the trachea, and the lungs were gently lavaged with 1 mL of sterile phosphate- buffered saline (PBS). The lavage fluid was immediately withdrawn to collect BALF samples. BALF samples were centrifuged at 3,200 rpm for 5 minutes at 4°C, and the supernatant was collected for analysis. Total protein concentration in BALF samples was determined using the Bradford assay (Bio- Rad, cat#5000006) according to the manufacturer's instructions. Fecal Sample Collection: fresh fecal samples were collected and immediately flash-frozen in liquid nitrogen, then stored at -80°C until further analysis. Metabolomics analysis was performed on samples collected from seven (n=7) mice, which served as biological replicates for the study. Comprehensive metabolomics profiling was conducted by Metabolon, Inc. (Morrisville, NC, USA) using their established global metabolomics platform. The analytical approach employed ultra-high performance liquid chromatography coupled with tandem mass spectrometry (UHPLC-MS / MS), utilizing four complementary analytical methods to maximize metabolome coverage: UHPLC-MS / MS (+ESI)1, UHPLC-MS / MS (+ESI)2, UHPLC- MS / MS (-ESI), and UHPLC(HILIC)-MS / MS. Quality control measures included the analysis of process blanks, pooled matrix samples as technical replicates, and the addition of internal standards to monitor instrument performance throughout the analytical run. Statistical analysis All statistical analyses were performed using GraphPad Prism 9 (GraphPad Software, Inc., California) statistical software packages. An unpaired equal variance Student’s t-test was used to compare the differences between groups for nonparametric data. A two-sided p-value of less than 0.05 was considered to be statistically significant (*p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001). Docket No.103362-015WO1 Results SFB drives Th17 expansion and reprograms immune landscapes in intestinal and lung compartments. To investigate the temporal dynamics of how segmented filamentous bacteria (SFB) colonization modulates host immune responses, C57BL / 6 mice were administered SFB-positive fecal material via oral gavage and subsequently analyzed at 1-, 2-, and 3-week intervals post-inoculation. The experimental design focused on characterizing immune cell differentiation patterns at two critical anatomical sites: locally within the small intestine lamina propria (SILP), representing the primary interface where gut microbiota directly engages with the host immune system, and systemically in lung tissue, leveraging the well-established bidirectional communication with the gut. Given the documented restriction of SFB-specific Th17 cells to particular T cell receptor (TCR) repertoires characterized by distinct V-beta chain usage patterns—a hallmark indicative of specific recognition of SFB-derived antigens presented through MHC class II molecules—targeted analysis of Vβ+CD4+T cell populations as a marker of SFB-responsive immunity was conducted. Flow cytometric analysis revealed that SFB colonization following oral gavage resulted in significant and sustained increases in Vβ+CD4+T cell frequencies in both local SILP and systemic lung tissue compartments compared to SFB-free control groups. Notably, this expansion exhibited a time-dependent pattern with progressive enrichment observed over extended colonization periods, showing active and ongoing immune priming (Figure 1A). Further characterization of T cell differentiation dynamics under SFB colonization conditions revealed profound and coordinated immune profile alterations across both tissue compartments. Th17 cell frequencies demonstrated significant elevation in both SILP and lung tissues, with this enhancement occurring within both Vβ-CD4+and Vβ+CD4+T cell subpopulations (Figure 1B). This broad expansion indicates that while SFB-specific Vβ+ cells show the most dramatic response, the overall Th17 milieu is enhanced, suggesting both direct antigen-specific activation and bystander activation mechanisms. Recent evidence demonstrates that Th17 cells can acquire IFN-γ production capabilities and express T-bet, particularly in inflammatory environments where IL-12 signaling predominates and TGF-β is reduced. This Th17-to-Th1 plasticity has been implicated in enhanced antimicrobial immunity and antitumor responses, showing that SFB-induced Th17 cells similarly contribute to broader immune surveillance functions. In addition to the anticipated phenotypic changes in Th17 cell populations, the analysis revealed further layers of immune modulation. T-bet expression, the master transcription factor for Th1 cell differentiation, was significantly upregulated across multiple T cell subsets, including both Vβ-CD4+and Vβ+CD4+populations, as well as in CD8+T cells Docket No.103362-015WO1 specifically within lung tissue (Figure 1C). This unexpected finding shows that SFB colonization promotes not only Th17 responses but also primes the immune system toward enhanced Th1-type immunity, creating a more robust and versatile immune environment through both direct Th1 induction and Th17-to-Th1 transdifferentiation mechanisms. Collectively, these findings demonstrate that SFB colonization functions as a potent immunomodulatory factor that extends far beyond local gut immunity. Similar to other commensal bacterial species, SFB enhances immune responses through mechanisms that involve both antigen-specific T cell activation and broader systemic immune reprogramming. Expression of SFB epitope in cancer cells reduces metastatic tumor burden and enhances Th17 cell infiltration in a lung metastasis model It was previously demonstrated a TCR enriched in Th17 cells (called 7B8 TCR) and mapped an I-Ab-restricted epitope (referred to as 3340), a unique SFB protein. The B16 melanoma cell line is a widely used transplantable tumor model. This cell line can be used to grow tumors in the lung when injected intravenously. To evaluate the functional consequences of SFB-driven immune responses in vivo, B16F1 melanoma cells were engineered to express the SFB3340 epitope, which facilitates Th17 cells into the tumors and triggers robust SFB-induced immune activation. Two experimental cell lines were generated: B16F13340(expressing the SFB3340 epitope) and B16F1MEM(control lacking the epitope). C57BL / 6 mice were preconditioned with either SFB-positive fecal material or PBS control via oral gavage for two weeks to establish differential gut colonization status. Subsequently, mice received an intravenous injection of either B16F13340or B16F1MEMcells to establish a metastatic lung cancer model, with analysis performed on day 20 post-tumor inoculation (Figure 2A). Remarkably, the combination of SFB3340 epitope expression and SFB colonization resulted in a dramatic reduction in pulmonary tumor burden compared to all control groups (Figure 2B). Quantitative assessment of lung tumor nodules demonstrated significant anti-tumor efficacy when both the SFB epitope and gut colonization were present, showing a synergistic interaction between epitope recognition and microbiota-primed immunity. Flow cytometric analysis of tumor-infiltrating lymphocytes revealed that SFB+B16F13340- transplanted mice exhibited significantly elevated frequencies of IL-17A+CD4+T cells compared to either SFB- B16F13340 or B16F1MEM control groups (Figure 2C, 2D). This finding confirms that the presence of the SFB3340 epitope on cancer cells, in conjunction with SFB gut colonization, synergistically promotes Th17 cell differentiation and recruitment within the metastatic tumor microenvironment. The enhanced Th17 response shows successful antigen presentation of the Docket No.103362-015WO1 bacterial epitope by tumor cells to SFB-primed T cells, creating a bridge between commensal bacterial immunity and anti-tumor responses. Beyond the expected IL-17A production driven by SFB3340 epitope recognition, the analysis revealed that this bacterial epitope conferred superior tumor immunogenicity, as evidenced by robust production of key anti-tumor cytokines TNF-α and IFN-γ in CD4+T cells (Figure 2C, 2D). This multifaceted cytokine response indicates that SFB3340 epitope recognition not only activates Th17- specific pathways but also enhances broader anti-tumor immunity, potentially involving Th1-type responses. The coordinated production of IL-17A, TNF-α, and IFN-γ shows that a comprehensive immune activation suppresses tumor growth and metastasis. SFB antigen increases tumor immunogenicity and enhances anti-tumor immune responses Th17 cells mediate antitumor responses through a dual mechanism: facilitating the recruitment of pro-inflammatory immune cells (macrophages, neutrophils, NK cells, and CD8+T cells) and limiting the accumulation of immunosuppressive myeloid-derived suppressor cells. Flow cytometric analysis of tumor-infiltrating lymphocytes revealed profound alterations in multiple immune cell populations that collectively enhanced anti-tumor capacity in B16F13340 mice compared to B16F1MEM controls. Detailed analysis of CD8+T cell populations revealed significant functional enhancement in B16F13340mice, with the frequencies of IFN-γ+and IL-17A+CD8+T cells markedly increased compared to control groups, indicating robust activation of both Tc1 and Tc17 effector programs (Figure 3A). Notably, TNF-α production by CD8+T cells remained unchanged, showing selective activation of specific cytotoxic pathways rather than generalized inflammatory responses. This dual cytokine profile indicates that SFB3340 epitope recognition promotes a multifaceted CD8+T cell response characterized by enhanced type 1 immunity (IFN-γ) and IL-17-mediated inflammatory responses, both critical for effective anti-tumor immunity. The SFB3340 epitope also elicited significant changes in the natural killer (NK) cell compartment within the tumor microenvironment, with both the absolute frequency of NK cells and the proportion of IFN-γ- producing NK cells substantially elevated in response to SFB3340 epitope expression (Figure 3B, 3C). This NK cell activation represents a crucial component of innate anti-tumor immunity, as activated NK cells can directly eliminate tumor cells through cytotoxic mechanisms and contribute to adaptive immune responses through the secretion of IFN-γ. Given that Gr-1 cells represent a hallmark population of myeloid-derived suppressor cells (MDSCs) known to prioritize pro-tumor functions through migration to invasive tumor fronts and facilitation of tumor cell invasion and metastasis, we conducted a detailed analysis of myeloid cell infiltration patterns (39, 40). Remarkably, B16F13340mice exhibited a significant reduction in Gr-1int Docket No.103362-015WO1 cell frequencies compared to B16F1MEMcontrol groups, representing a critical shift in the tumor immune landscape, as reduced MDSC infiltration typically correlates with enhanced immune surveillance and improved anti-tumor responses. Additionally, dendritic cell (DC) populations were significantly increased in B16F13340 mice, further supporting enhanced antigen presentation and T cell activation within the tumor microenvironment (Figure 3D). The coordinate changes across multiple immune cell lineages create a comprehensively reprogrammed tumor microenvironment characterized by enhanced effector cell and immune surveillance function with reduced immunosuppression. SFB antigen bridges gut-tumor immunity To elucidate the mechanistic relationship between SFB3340 epitope expression, gut colonization status, and anti-tumor efficacy, a comprehensive correlation analyses was performed between critical anti-tumor immune cell populations and pulmonary tumor burden. Quantitative assessment revealed that B16F13340tumors exhibited robust negative correlations with tumor nodule counts across multiple key tumoricidal cell populations within the tumor microenvironment (Figure 4). Specifically, strong inverse associations were observed between tumor burden and the frequencies of IFN-γ-producing CD4+T cells, CD8+T cells, and NK cells, indicating that enhanced type 1 immune responses directly correspond to reduced metastatic tumor establishment. Similarly, TNF-α- producing CD4+and CD8+T cells demonstrated significant negative correlations with tumor counts, underscoring the importance of pro-inflammatory cytokine production in mediating anti-tumor immunity. Notably, IL-17A+CD8+T cells also showed strong inverse correlations with tumor burden, confirming the anti-tumor potential of Tc17 responses in this melanoma model and supporting the therapeutic value of IL-17-mediated immune activation. The integration of SFB3340 epitope presentation on melanoma cells with SFB gut colonization created a synergistic immunological platform that substantially amplified anti-tumor immune responses beyond what could be achieved by either component alone. The observed correlations show that SFB-derived antigens, when presented in the context of tumor-associated antigens, can effectively bridge commensal bacterial immunity and anti-tumor responses, resulting in a comprehensive immune activation state that translates into measurably improved clinical outcomes. SFB-mediated multi-tissue metabolic reprogramming enhances anti-tumor immunity The present disclosure shows that SFB colonization further strengthens anti-tumor immune responses. Next, it was investigated whether SFB modulates immune system function through alterations in metabolic homeostasis in vivo. A comprehensive global metabolite profiling was Docket No.103362-015WO1 conducted across multiple biological compartments. Untargeted metabolomics analysis was performed to characterize metabolite perturbations between SFB-negative and SFB-positive mice, providing insight into the biochemical mechanisms underlying microbiota-immune interactions. Biological samples were systematically obtained from seven mice in each of five experimental groups (n=7 / group), yielding biological replicates for comprehensive metabolomics profiling: naïve controls, SFB-colonized mice, B16F13340 tumor-bearing mice, SFB-colonized B16F13340 tumor-bearing mice (SFB+B16F13340), and SFB-colonized B16F1MEM control tumor-bearing mice (SFB+B16F1MEM), enabling a comprehensive assessment of metabolic alterations across different colonization and tumor contexts (Figure 5A). Principal component analysis (PCA) was applied to the complete metabolomics dataset to visualize global metabolic patterns and identify systematic differences between experimental groups. The PCA revealed distinct clustering patterns that clearly segregated SFB- negative from SFB-positive individuals, indicating that SFB colonization induces profound and reproducible changes in host metabolism that can be detected across the entire metabolome (Figure 5B). For identification of significantly altered metabolites, a stringent statistical criterion was employed, selecting compounds that exhibited fold changes > 2.0 for upregulated metabolites or <0.5 for downregulated metabolites, followed by filtering for statistical significance (p-value <0.05). Focused comparison between B16F13340 and SFB+B16F13340 groups revealed extensive metabolic reprogramming across multiple physiological compartments, including bronchoalveolar lavage fluid (BALF), serum, and fecal samples (Figures 5C, 5D). This multi-tissue metabolomics signature indicates that SFB colonization induces coordinated metabolic changes that span local gut metabolism, systemic circulation, and respiratory tract biochemistry, showing that the metabolic influence of SFB extends far beyond the initial site of colonization to affect whole-body metabolic homeostasis and potentially contribute to the observed immune system modulation and enhanced anti-tumor responses. To elucidate the specific metabolic mechanisms underlying SFB-mediated enhancement of anti-tumor immunity, a detailed analysis of the top 10 most significantly upregulated metabolites across all tissue compartments was conducted in SFB-colonized B16F13340 tumor-bearing mice compared to non-colonized controls. Metabolite intensities were visualized using heatmap analysis with z-score standardization to enable direct comparison of metabolite abundance patterns across different organs and tissues, with metabolites arranged according to fold-change magnitude from highest to lowest. Among the most prominently upregulated compounds, coordinated increases in metabolites were identified from the aromatic amino acid degradation pathway, including hippurate and its upstream precursor 3-phenylpropionate (highlighted in black), indicating enhanced microbial metabolism of phenylalanine and tyrosine. Additionally, significant elevation of p-cresol sulfate and Docket No.103362-015WO1 p-cresol glucuronide (highlighted in blue) was observed, both representing conjugated derivatives of the microbial metabolite p-cresol and reflecting enhanced host phase II detoxification processes (Figure 5E). Previous studies also showed that hippuric acid was significantly elevated in responders compared with non-responders within non-small cell lung cancer cohorts treated with PD-1 blockade therapy. These metabolites represent a novel approach to predicting ICB response by focusing on host immune metabolic status, offering a more comprehensive and patient-friendly biomarker strategy for immunotherapy. Discussion The immunological role of Th17 cells in tumor biology remains a subject of ongoing debate, with evidence supporting both pro-tumorigenic and anti-tumorigenic functions. On one hand, numerous studies have demonstrated that Th17 cells can promote tumor progression by facilitating angiogenesis, enhancing tumor cell migration and metastasis, recruiting regulatory T cells (Tregs), and secreting immunosuppressive cytokines such as IL-10 and TGF-β. These activities contribute to the establishment of a tumor-permissive microenvironment and are associated with poor prognosis in several cancer types. Conversely, substantial research has also highlighted the capacity of Th17 cells to mediate anti-tumor immunity. Th17 cells can secrete effector cytokines like IL-17, which are implicated in the recruitment of antitumor macrophages and the activation of cytotoxic immune cells, including CD8+ T cells and natural killer (NK) cells. Furthermore, the plasticity of Th17 cells allows them to adopt Th1-like phenotypes, thereby enhancing their tumoricidal potential through the production of IFN-γ and other pro-inflammatory mediators. To explore the therapeutic implications of Th17 responses within the tumor microenvironment, SFB was employed to selectively induce Th17 cell activation in a metastatic lung cancer model. Specifically, the B16F1 melanoma cell line was engineered to express the SFB epitope SFB3340, which robustly stimulates Th17 cells. This targeted activation resulted in pronounced anti- tumor effects, characterized by increased production of effector cytokines from CD4⁺ and CD8⁺ T cells, as well as NK cells within the tumor milieu. These findings underscore the harnessing of microbiota-driven Th17 responses to enhance anti-tumor immunity and inform the development of novel immunotherapeutic strategies. The metabolomics analysis, herein, further revealed that SFB colonization has a consistent and systemic metabolic impact across multiple organs. Metabolites such as hippurate, which are upregulated in the gut in the presence of SFB, were also significantly elevated in other compartments, including bronchoalveolar lavage fluid (BALF) and serum. Previous studies identified a set of plasma Docket No.103362-015WO1 metabolites, including hippuric acid (a microbiome-derived metabolite) achieved high predictive accuracy (AUC = 0.91) for response to therapy. Additionally, a combination of T cell markers—such as mitochondrial activation and the frequencies of CD8⁺PD-1hi and CD4⁺ T cells—yielded even greater predictive value (AUC = 0.96) (41). In the context of PD-1 blockade therapy, elevated hippuric acid levels have been associated with enhanced antitumor immunity and improved clinical responses, likely due to the interplay between microbiota-derived metabolites and host immune cell activation. In summary, these findings underscore the significance of SFB microbiota-induced Th17- mediated antitumor immunity in the context of metastatic lung tumors, revealing its capacity to modulate metabolic pathways and foster homeostasis across multiple tissues. These insights advance our understanding of how the SFB-Th17 immune axis contributes to enhanced antitumor responses and support the ongoing development of commensal bacteria-based cancer vaccines and microbiota- targeted therapeutic strategies. It will be apparent to those skilled in the art that various modifications and variations can be made in the present disclosure without departing from the scope or spirit of the invention. Other embodiments of the disclosure will be apparent to those skilled in the art from consideration of the specification and practice of the methods disclosed herein. It is intended that the specification and examples be considered as exemplary only, with a true scope and spirit of the invention being indicated by the following claims.

[0002] Docket No.103362-015WO1 TABLES Table 1. Antibodies used.

[0003] Docket No.103362-015WO1 SEQUENCES 1. SEQ ID NO: 1 - SFB epitope QFSGAVPNK 2. SEQ ID NO: 2 – SFB736F GACACTGAGGCATGAGAGCAT 3. SEQ ID NO: 3 - SFB844R GACGGCACGGATTGTTATTCA 4. SEQ ID NO: 4 – UnitF340 ACTCCTACGGGAGGCAGCAGT 5. SEQ ID NO: 5 – UnitR514 ATTACCGCGGCTGCTGGC 6. SEQ ID NO: 6 - SFB3340 peptide ATVNSNKSNNNDLVFDVQFSGAVPNKTDASWILDING

Claims

Docket No.103362-015WO1 CLAIMS What is claimed is:

1. An immunotherapeutic composition comprising a commensal bacterial antigen and a pharmaceutically acceptable carrier, wherein the commensal bacterial antigen comprises an epitope derived from a Segmented Filamentous Bacterium (SFB).

2. The immunotherapeutic composition of claim 1, wherein the epitope comprises a polypeptide expressed by the SFB.

3. The immunotherapeutic composition of claim 1 or 2, wherein the epitope comprises a SFBNYU_003340 SFB polypeptide.

4. The immunotherapeutic composition of any one of claims 1-3, wherein the epitope comprises SEQ ID NO: 1, or a fragment thereof.

5. A method of treating a cancer in a subject in need thereof, the method comprising administering to the subject an immunotherapeutic composition comprising a commensal bacterial antigen and a pharmaceutically acceptable carrier, wherein the commensal bacterial antigen comprises an epitope derived from a Segmented Filamentous Bacterium (SFB).

6. The method of claim 5, wherein the epitope comprises a polypeptide expressed by the SFB.

7. The method of claim 5 or 6, wherein the epitope comprises a SFBNYU_003340 SFB polypeptide.

8. The method of any one of claims 5-7, wherein the epitope comprises SEQ ID NO: 1, or a fragment thereof.

9. The method of any one of claims 5-8, wherein the immunotherapeutic composition is administered in combination with an immunotherapy.

10. The method of claim 9, wherein the immunotherapy comprises a chimeric antigen receptor (CAR), a monoclonal antibody, an immune checkpoint inhibitor (ICI), or a combination thereof.Docket No.103362-015WO1 11. The method of any one of claims 5-10, wherein the method enhances an immune response to the immunotherapy.

12. The method of any one of claims 5-11, wherein the method increases one or more T cells in the subject.

13. The method of claim 12, wherein the one or more T cells comprises a CD4 T cell or a CD8 T cell.

14. The method of any one of claims 5-13, wherein the method reduces or prevents tumor growth in the subject.

15. The method of any one of claims 5-14, wherein the cancer comprises a melanoma or a lung cancer.

16. The method of any one of claims 5-15, wherein the cancer comprises a metastatic cancer.

17. A method of preventing or reducing tumor growth in a subject in need thereof, the method comprising administering to the subject an immunotherapeutic composition comprising a commensal bacterial antigen and a pharmaceutically acceptable carrier, wherein the commensal bacterial antigen comprises an epitope derived from a Segmented Filamentous Bacterium (SFB).

18. The method of claim 17, wherein the epitope comprises a polypeptide expressed by the SFB.

19. The method of claim 17 or 18, wherein the epitope comprises a SFBNYU_003340 SFB polypeptide.

20. The method of any one of claims 17-19, wherein the epitope comprises SEQ ID NO: 1, or a fragment thereof.

21. The method of any one of claims 17-20, wherein the immunotherapeutic composition is administered in combination with an immunotherapy.Docket No.103362-015WO1 22. The method of claim 21, wherein the immunotherapy comprises a chimeric antigen receptor (CAR), an immune checkpoint inhibitor (ICI), or a combination thereof.

23. The method of any one of claims 17-22, wherein the method enhances an immune response to the immunotherapy.

24. The method of any one of claims 17-23, wherein the method increases one or more T cells in the subject.

25. The method of claim 24, wherein the one or more T cells comprises a CD4 T cell or a CD8 T cell.

26. The method of any one of claims 17-25, wherein the method treats or prevents a cancer in the subject.

27. The method of any one of claims 17-26, wherein the cancer comprises a melanoma or a lung cancer.

28. The method of any one of claims 17-27, wherein the cancer comprises a metastatic cancer.

29. A method of enhancing an immunotherapy in a subject, the method comprising administering to the subject an immunotherapeutic composition comprising a commensal bacterial antigen and a pharmaceutically acceptable carrier, wherein the commensal bacterial antigen comprises an epitope derived from a Segmented Filamentous Bacterium (SFB).

30. The method of claim 29, wherein the epitope comprises a polypeptide expressed by the SFB.

31. The method of claim 29 or 30, wherein the epitope comprises a SFBNYU_003340 SFB polypeptide.

32. The method of any one of claims 29-31, wherein the epitope comprises SEQ ID NO: 1, or a fragment thereof.Docket No.103362-015WO1 33. The method of any one of claims 29-32, wherein the immunotherapy comprises an immune checkpoint inhibitor, a monoclonal antibody, a chimeric antigen receptor (CAR), or a combination thereof.

34. The method of any one of claims 29-33, wherein the method increases one or more T cells in the subject.

35. The method of claim 34, wherein the one or more T cells comprises a CD4 T cell or a CD8 T cell.

36. The method of any one of claims 29-35, wherein the method treats or prevents a cancer in the subject.

37. The method of any one of claims 29-36, wherein the cancer comprises a melanoma or a lung cancer.

38. The method of any one of claims 29-37, wherein the cancer comprises a metastatic cancer.

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