167 results about "Self-Antigens" patented technology

This invention relates to a vaccine and a method for immune activation which is effective for eliciting both a systemic, non-antigen specific immune response and a strong antigen-specific immune response in a mammal. The method is particularly effective for protecting a mammal from a disease including cancer, a disease associated with allergic inflammation, an infectious disease, or a condition associated with a deleterious activity of a self-antigen. Also disclosed are therapeutic compositions useful in such a method.

This invention relates to a vaccine and a method for immune activation which is effective for eliciting both a systemic, non-antigen specific immune response and a strong antigen-specific immune response in a mammal. The method is particularly effective for protecting a mammal from a disease including cancer, a disease associated with allergic inflammation, an infectious disease, or a condition associated with a deleterious activity of a self-antigen. Also disclosed are therapeutic compositions useful in such a method.

This invention provides novel methods of obtaining autologous monoclonal antibodies (AMABs) to self-antigens or homologs thereof. The method involves obtaining a genetically engineered host animal that does not biosynthesize at least one epitope of the antigen and utilizes the lack of self-tolerance of the host to the epitope to produce antibodies specific to the antigen. The invention also encompasses the AMABs produced by the methods. The invention further encompasses methods of isolating cells comprising the use of such AMABs that have specificity for a cell surface antigen.

Disclosed herein are compositions and methods for eliciting immune responses against antigens. In particular embodiments, the compounds and methods elicit immune responses against antigens that are otherwise recognized by the host as “self” antigens. The immune response is enhanced by presenting the host immune system with a chimeric antigen comprising an immune response domain and a target binding domain, wherein the target binding domain comprises a xenotypic antibody fragment. By virtue of the target binding domain, antigen presenting cells take up, process, and present the chimeric antigen, eliciting both a humoral and cellular immune response.

Provided herein are novel panels of biomarkers for the detection and diagnosis of lung adenocarcinoma, and methods and kits for detecting these biomarkers in samples of individuals suspected of having the disease. Also provided are methods of monitoring the progression of lung adenocarcinoma and methods of monitoring the efficacy of a treatment.

Biomarkers for liver diseases and method for using the same are provided. For detecting liver cirrhosis and liver cancer, the biomarkers are selected from any one of the amino acid sequences with SEQ ID NO:1 to SEQ ID NO:24 or derivatives or fragments or variants or the combination thereof or the antibodies against the amino acid sequences. Then the biomarkers are further developed into detection kits, such that by detecting the existence of autoantibodies or autoantigens in screened specimens, liver diseases are detected with higher accuracy and sensitivity.

The invention provides methods for treating autoimmunity and for reestablishing tolerance. The methods involve the coadministration of anti-CD3 antibodies and self-antigens. The coadministration has the potential to provide a synergistic effect of protecting or reducing autoaggressive immune processes and/or of reestablishing tolerance towards self-antigens. An underlying rationale behind the methods is that the administration of self-antigens together with anti-CD3 antibodies can alter the response to those self-antigens and prevent progression of autoimmunity. By rechallenging with the autoantigens and stimulating the non-pathogenic response, the blockade of the autoimmune process can be maintained. Preclinical evidence provided herein shows that the combination of anti-CD3 and autoantigen is synergistic in reversing autoimmune diabetes, and therefore, suggests that combination therapy of anti-CD3 and self-antigen may provide synergistic protection in reversing other autoimmune disorders.

Systemic lupus erythematosus (SLE) can be prevented or treated by down-regulating the autoimmune response to the C-terminal-DNA-binding domain of the p53 protein (p53) by an active principle selected from the group consisting of: (i) a peptide of, or comprising, the C-terminal DNA-binding domain of the p53 protein; (ii) a monoclonal antibody (mAb) specific for said domain of p53 (Ab1), and fragments thereof; (iii) an mAb specific for Ab1 (hereinafter Ab2), and fragments thereof; (iv) a peptide based on a complementarity determining region (CDR) of the heavy or light chain of said Ab1 or Ab2; (v) a DNA molecule coding for (i) and (iv) of for the variable region of said Ab1 and Ab2 of (ii) and (iii); and (vi) T cells specific for (i) to (iv), fragments thereof, T cell receptor (TCR) thereof and peptides comprising the variable region of said TCR. SLE can also be diagnosed by assaying for antibodies (Ab1) against the C-terminal DNA-binding domain of p53 or antibodies (Ab2) specific to the Ab1 antibodies.

A pro-inflammatory T cell response is specifically suppressed by the injection into a recipient of DNA encoding an autoantigen associated with autoimmune disease. The recipient may be further treating by co-vaccination with a DNA encoding a Th2 cytokine, particularly encoding IL4. In response to the vaccination, the proliferation of autoantigen-reactive T cells and the secretion of Th1 cytokines, including IL-2, IFN-γ and IL-15, are reduced.

Provided are viral display vehicles which display multiple sclerosis associated antigens on the surface thereof for induction of immune tolerance to autoantigens such as MOG. Also provided are methods and pharmaceutical compositions for treating multiple sclerosis using the viral display vehicles of the present invention.

Mutations to the tumor suppressor protein p53 have been observed in 40-60% of all human cancers. These mutations are often associated with high nuclear and cytoplasmic concentrations of p53. Since many tumors exhibit highly elevated p53 levels, the protein is an attractive target for cancer immunotherapy. Unfortunately, p53 is an autoantigen that is likely to be tolerated as a self-protein by the immune system. The present invention is based on the discovery that this self-tolerance can be overcome by administration of recombinant modified vaccinia Ankara (MVA) containing a nucleic acid that encodes p53 (rMVAp53). The invention discloses a method of generating a p53-specific CTL-response to tumor cells expressing mutated p53 by administering a composition comprising rMVAp53. Administration of rMVAp53 decreases tumor development, tumor growth, and mortality in a variety of malignant cell types. These effects are enhanced by administration of CTLA-4 blocker and/or CpG oligodeoxynucleotide immunomodulators.

The present invention provides a method of selectively augmenting an immunosuppressive function in various functions of NKT cells, and a method of efficiently inducing an antigen specific immunosuppression in vivo, as well as a pharmaceutical obtained by applying the same.

More particularly, the present invention provides a pharmaceutical (e.g., a preventive or therapeutic agent for immune diseases such as allergic disease and autoimmune disease) containing a CD1d ligand and a target antigen (e.g., allergen, autoantigen). Preferably, the pharmaceutical contains a drug delivery vehicle including the CD1d ligand and the target antigen and having a lumen.

The present invention relates to a stereochemically based “non-self” antigen vaccine for the prevention and/or treatment of Alzheimer's and other amyloid related diseases. The present invention provides a vaccine for the prevention and treatment of Alzheimer's and other amyloid related diseases, which overcomes the drawbacks associated with using naturally occurring peptides, proteins or immunogens.

The invention is directed to a method of treating a T cell-mediated autoimmune disease in animals, including humans, by the oral administration of autoantigens, fragments of autoantigens, or analogs structurally related to those autoantigens, which are specific for the particular autoimmune disease. The method of the invention includes both prophylactic and therapeutic measures.

The methods include selectively reducing or expanding T cells according to the antigenic specificity of the T cells using biocompatible bioabsorbable nanospheres. Therefore, the present invention can be used to reduce or eliminate pathogenic T cells that recognize autoantigens, such as beta cell specific T cells. As such, the present invention can be used to prevent, treat or ameliorate autoimmune diseases such as IDDM. Furthermore, the present invention can be used to expand desirable T cells, such as anti-pathogenic T cells to prevent, treat and/or ameliorate autoimmune diseases.

Novel compositions are disclosed which can induce or enhance an immune response against foreign or self antigens (microbial or parasitic) or modulate (that can lead to suppression) the activity of pathogenic cells in inflammatory or autoimmune diseases. Compositions and methods are taught in how to limit the generation of an immune response against formulated peptides and proteins with application in antibody therapy or hormone replacement therapy. Methods of suppressing autoimmunity are also disclosed which use ligands for cellular receptors expressed on cells of the innate immune system and more specifically for down-regulation of autoimmune processes by either deletion or induction of anergy at the level of autoreactive T cells or by triggering active-suppressor T cells that down-regulate the activity of pathogenic cells.

Stimulation of T cells to respond to self antigens is achieved through a blockade of CTLA-4 signaling. CTLA-4 blocking agents are combined with antigen preparations, either alone or with additional immune response stimulating agents, in costimulation strategies to break immune tolerance and stimulate an enhanced T-cell response against self antigens. This enhanced response is useful for the treatment of non-immunogenic and poorly-immunogenic tumors, as well as other medical conditions requiring selective tissue ablation.

The present invention provides a method of producing autoantigens, compositions comprising autoantigenic fragments and methods of using autoantigenic fragments in the treatment of a condition associated with an autoimmune response. Also provided are assays for the detection or assessment of an autoimmune response.

Methods of inducing T cell proliferation and expansion in vivo for treating conditions wherein antigen-specific T cell immune response are therapeutically desirable such as cancer, infection, inflammation, allergy and autoimmunity and for enhancing the efficacy of vaccines are provided. These methods comprise the administration of at least one CD27 agonist, preferably an agonistic CD27 antibody, alone or in association with another moiety such as immune stimulant or immune modulator such as an anti-CD40, OX-40, 4-IBB, or CTLA-4 antibody or an agent that depletes regulatory cells, or a cytokine. These mono and combination therapies may also optionally include the administration of a desired antigen such as a tumor antigen, an allergen, an autoantigen, or an antigen specific to an infectious agent or pathogen against which a T cell response (often CD8+) is desirably elicited.

The present invention provides compositions and methods for specifically inhibiting host immune responses against autoantigens. In particular, compositions and methods combining CD8 polypeptide expression with autoantigen expression or presentation are described for specifically inhibiting the humoral and cellular components of the host immune response to autoantigens.

Co-administration of an effective amount of autoantigen and UV light to mucosal associated lymphatic tissue (MALT) in a patient.