48 results about "Cd4 t cell" patented technology

The invention provides methods of identifying naïve T cells by expression of PTK7.

The present invention relates to recombinant acetylcholine receptor polypeptides recognized by CD4 T cells of a myasthenia gravis patient and compositions for the treatment of myasthenia gravis containing the same as an effective ingredient, more precisely, recombinant acetylcholine receptor polypeptides deficient in B cell epitope, recombinant acetylcholine polypeptides in which two or more T cell epitopes are fused, a composition for the treatment of myasthenia gravis containing the above recombinant polypeptides as an effective ingredient and a treatment method for myasthenia gravis using the composition. The composition containing one or more recombinant polypeptides above can be effectively used as a myasthenia gravis specific therapeutic agent or immunomodulator without side effects.

Cytotoxic T lymphocytes (CTLs) specific for antigenic peptides derived from IgE molecule can be generated in vitro by stimulating resting naive CD8 T cells with IgE peptides presented by artificial antigen presenting cells. The IgE specific CTLs lyse the target cells loaded with IgE peptides in vitro and inhibit antigen specific IgE response in vivo. In addition, adoptive transfer of the IgE specific CTL to an asthmatic mouse model can inhibit the development of lung inflammation and airway hypersensitivity. IgE specific CTL provides a treatment for allergic asthma and other IgE-mediated allergic diseases. Antigenic peptides identified from non-tumor self-antigens induce specific cytotoxic T lymphocyte (CTL) in vitro. The CTL induced by peptides identified from CD40L can kill activated CD4 T cells. In vitro generated CTL specific for CD40L inhibit CD4-dependent antibody responses of all isotypes in vivo. In contrast, CTL induced by antigenic peptides derived from IgE specifically inhibit IgE responses, and adoptive transfer of CD40L-specific CTL to NOD mice at early age delay the development of diabetes in NOD mice. In vitro generated CTL specific for non-tumor self-antigens expressed on activated CD4 T cells regulate immune responses in vivo.

The invention discloses a DN T cell transformation and multiplication method which comprises the following steps: (1) extracting mononuclear cells in an initial sample, and removing CD8<+>T cells and NK cells from the mononuclear cells; (2) culturing the sample obtained in the step (1) in vitro with a culture medium containing a T cell stimulant and cell factors; adding an OX40 activated antibody or an OX40 ligand at the same time in the culturing process; (3) purifying DN T cells after 5-7 days' culture. The method can be implemented without purifying CD4<+>T cells or natural DN T cells, so that the operation difficulty is reduced, the operation efficiency is improved, and the culture period is short; the apoptosis rate of DN T cells in multiplication can be effectively reduced, and the immunosuppression function can be improved; the DN T cell yield is greatly improved as compared with that in the prior art; the obtained DN T cells have remarkable immunosuppression function, the percentage of the proliferated CD4 T cells is reduced to 2.94% as compared with that in the prior art, and the suppression ratio can reach 93%.

The present invention relates to a polynucleotide encoding CDR3 in the TCR-α chain and TCR-β chain genes of CD4+ helper T cells specific for a WT1 helper peptide having the amino acid sequence of SEQ ID NO: 123 . The invention also relates to the peptides encoded by said polynucleotides. The present invention also relates to CD4+T cells into which the TCR gene containing the polynucleotide has been introduced, the use of CD4+T cells to induce WT1-specific cytotoxic T-lymphocytes (CTL), cancer treatment, and the like.