The present invention provides a composition comprising dendritic cells loaded with hHsp60sp, which dendritic cells are from a subject and have been fixed with paraformaldehyde (PFA). The subject may suffer from an autoimmune disease. Also provided are a method for preparing the composition; recombinant human cells comprising a heterologous gene encoding a fusion protein of HLA-E and hHsp60sp or B7sp, and expressing the fusion protein on the surface of the cells; a method for determining a percentage of maximum inhibition of testing the function of the HLA-E restricted CD8+ Treg cells from a subject, determining whether HLA-E restricted CD8+ Treg cells freshly isolated from a subject are defective, or determining whether defective HLA-E restricted CD8+ Treg cells from a subject are correctable; and a method for correcting defective HLA-E restricted CD8+ Treg cells, treating type 1 diabetes (T1D), or treating multiple sclerosis (MS).

The present invention relates to pharmaceutical vaccine compositions comprising at least one vaccine antigen together with living immune cells. These immune cells include at least a portion of activated T-cells and act as an adjuvant. Methods for using these pharmaceutical compositions to prevent or treat diseases, such as cancer, infectious diseases and autoimmune disease are also included.

A method is provided for preventing rejection by an immune system of a recipient subject of a tissue transplanted from a donor subject into the recipient subject without the need for long-term administration of non-specific immunosuppressive drugs.

Methods are provided for inhibiting or enhancing down-regulation of an antigen-activated HLA-E.sup.+ T cell by an HLA-E-restricted CD8.sup.+ T cell comprising contacting the HLA-E.sup.+ T cell and CD8.sup.+ T cell with an agent which inhibits or enhances, respectively, binding between (i) T cell receptor (TCR) on the surface of the CD8.sup.+ T cell and (ii) a self peptide presented by HLA-E on the surface of the HLA-E.sup.+ T cell, thereby inhibiting or enhancing, respectively, down-regulation of the antigen-activated HLA-E.sup.+ T cell. Compositions comprising agents which inhibit or enhance/activate, respectively, binding between (i) T cell receptor (TCR) on the surface of a CD8 T cell and (ii) a self peptide presented by HLA-E on the surface of a HLA-E.sup.+ T cell, and assays for identifying such agents, are provided.

Provided herein are cells expressing a first and a second chimeric protein in the cell membrane. Such cells can solve expression problems of CAR constructs caused by these CAR construct's ability to recognize unwanted internal epitopes or exhibiting unwanted signalling due to misfolding/scFv aggregation. The first chimeric protein comprises an extracellular antigen binding unit and an intracellular dimerization domain. The second chimeric protein comprises a lipid anchoring domain, an intracellular dimerization domain and a signaling domain. Accordingly, the expression of the two proteins allows them to translocate to the cell membrane without much interference and subsequently gain signaling capacity when colocalized at the cell membrane.

The present invention provides a peptide containing 8 or more consecutive amino acid residues in an amino acid sequence of any of SEQ ID NOS: 1 to 15 and consisting of 11 or less amino acid residues.

The present invention provides a composition comprising dendritic cells loaded with hHsp60sp, which dendritic cells are from a subject and have been fixed with paraformaldehyde (PFA). The subject may suffer from an autoimmune disease. Also provided are a method for preparing the composition; recombinant human cells comprising a heterologous gene encoding a fusion protein of HLA-E and hHsp60sp or B7sp, and expressing the fusion protein on the surface of the cells; a method for determining a percentage of maximum inhibition of testing the function of the HLA-E restricted CD8+ Treg cells from a subject, determining whether HLA-E restricted CD8+ Treg cells freshly isolated from a subject are defective, or determining whether defective HLA-E restricted CD8+ Treg cells from a subject are correctable; and a method for correcting defective HLA-E restricted CD8+ Treg cells, treating type 1 diabetes (T1D), or treating multiple sclerosis (MS).