4 results about "T helper cell" patented technology

The present invention relates to a composition, for prevention or treatment of cancer diseases, comprising CD8+ T cells activated by CD4+ T cell-derived extracellular vesicles as an active ingredient. It was found that the secretion of extracellular vesicles from cytokine-activated CD4+ T cells increases and the extracellular vesicles enhance proliferation and activity of CD8+ T cells to induce the death of cancer cells, thereby augmenting an anticancer effect. Thus, the present invention provides the CD8+ T cells activated by CD4+ T cell-derived extracellular vesicles as a pharmaceutical agent or an immunotherapeutic agent for cancer diseases, and a method for activating CD8+ T cells by using CD4+ T cell-derived extracellular vesicles to prepare CD8+ T cells showing excellent anticancer activity as described above.

Aging progresses at different rates among individuals, underscoring the need for better indicators of functional decline. The inventors showed that the T cell energy metabolism in the elderly reveals that high mitochondrial oxidative phosphorylation, especially in CD4 T regulatory cells, is associated with a reduced probability of being frail / prefrail, independent of age, sex, or comorbidities. When mitochondrial respiration drops below a critical threshold, it adversely affects intrinsic capacity. Furthermore, a low level of oxidative phosphorylation in CD4 T helper cells, particularly in central and effector memory subsets, was significantly associated with a faster decline in intrinsic capacity over time, suggesting that T cell mitochondrial bioenergetics represents a key biomarker for managing functional decline in older adults. Accordingly, the present invention relates to a method for determining the risk of age-related functional decline in a subject comprising the step of measuring the mitochondrial dependency in a population of T cells wherein the mitochondrial dependency (MitoDep) correlates with the age-related functional decline.

The present disclosure is directed to peptide immunogen constructs targeting the extracellular membrane-proximal domain of membrane-bound IgE (or IgE EMPD) and formulations thereof for the treatment of IgE-mediated allergic diseases. The IgE EMPD peptide immunogen constructs have a B cell epitope peptide of more than 20 amino acids, preferably cyclic, linked through an optional spacer to heterologous T helper cell (Th) epitopes derived from pathogen proteins. These peptide immunogen constructs and formulations thereof can stimulate the generation of highly specific antibodies in vaccinated hosts that are directed against the IgE EMPD peptide and are crossreactive with membrane-bound IgE on B lymphocytes committed to IgE secretion. The antibodies induced by the peptide immunogen constructs and formulations thereof in vaccinated hosts can induce apoptosis of IgE-expressing B cells and mediate Antibody Dependent Cellular Cytototoxity (ADCC), resulting in reduction of antigen-specific IgE and total IgE levels in vaccinated hosts to effectively treat IgE-mediated allergic pathology.

The present invention relates to a modified virus-like particle (VLP) of Cucumber Mosaic Virus (CMV) comprising at least one fusion protein, wherein the at least one fusion protein comprises or preferably consists of b) a chimeric CMV polypeptide, wherein the chimeric CMV polypeptide comprises or preferably consists of (iii) a CMV polypeptide, wherein the CMV polypeptide comprises a coat protein of CMV; and (iv) an antigen polypeptide, wherein the antigen polypeptide is inserted into the CMV polypeptide, wherein the insertion of the antigen polypeptide is between amino acid residues corresponding to position 84 and position 85 of SEQ ID NO: 62 of the CMV polypeptide; and (iii) a T helper cell epitope, wherein the T helper cell epitope replaces an N-terminal region of the CMV polypeptide, and wherein preferably the N-terminal region of the CMV polypeptide corresponds to amino acids 2-12 of SEQ ID NO: 62.