Abstract: The present invention provides a cytokine-based culture method for ex vivo expansion of NK cells from postembryonic hematopoietic stem cells into a fully closed, large-scale, cell culture bioprocess. We optimized enrichment of CD34+ cells followed by efficient expansion in gas-permeable cell culture bags. Thereafter, expanded CD34+ cells could be reproducibly amplified and differentiated into CD56+CD3? NK cell products with a mean expansion of more than 2,000 fold and a purity of >90%. Also provided are collections of cultured cells having specific properties.

Abstract: The invention describes a method and compounds for the prevention of immune responses towards allofactors, towards viral vectors used for gene therapy and gene vaccination, towards proteins to which subjects are naturally exposed, towards genetically-modified organisms and towards undesirable effects related to vaccine administration for allergic or infectious diseases.

Abstract: The disclosure features, inter alia, immunogenic XBP1-, CD138-, and CS1-derived peptides (and pharmaceutical compositions thereof). The peptides can be used in a variety of methods such as methods for inducing an immune response, methods for producing an antibody, and methods for treating a cancer (e.g., a plasma cell disorder such as multiple myeloma or Waldenstrom's macroglobulinemia). The peptides can also be included in MHC molecule multimer compositions and used in, e.g., methods for detecting a T cell in a population of cells.

Abstract: A composition for treating type 1 diabetes mellitus autoimmunity can include a therapeutically effective amount of two or more overlapping fragments of preproinsulin and a pharmaceutically acceptable carrier, wherein at least one of the polypeptide fragments is antigenic.

Abstract: The invention is related to peptide constructs, i.e.

Abstract: The invention provides anti-14-3-3 eta antibodies that specifically bind to the human 14-3-3 eta protein isoform in its natural configuration while exhibiting selectivity over human 14-3-3 alpha, beta, delta, epsilon, gamma, tau, and zeta protein isoforms. Methods, kits and pharmaceutical compositions comprising said specific anti-14-3-3 eta antibodies are further provided for the diagnosis and treatment of arthritis.

Abstract: The present invention relates to the use of immunogenic peptides comprising a T-cell epitope derived from an intracellular pathogen-associated antigen and a redox motif such as C-(X)2-[CST] or [CST]-(X)2-C in the prevention and/or treatment of infection with an intracellular pathogen and in the manufacture of medicaments therefore.

Abstract: Combinations of anti-cancer antibodies and inhibitory antibodies to CD223 overcome immune suppression in cancer patients. The inhibitory antibodies may be generated in an animal by injection of fragments of CD223. Antibodies may be monoclonal antibodies or single chain antibodies or humanized antibodies.

Abstract: The present disclosure relates to a method of preventing rheumatoid arthritis comprising administering a polynucleotide encoding Ssu72.

Abstract: The present invention relates to immunogenic peptides comprising a T-cell epitope. Said peptides are modified such that CD4+ T-cell responses are obtainable that are much stronger than the CD4+ T-cell responses obtained with the same peptides not comprising said modification. In particular, the modification is the addition of a cysteine, insertion of a cysteine or mutation into a cysteine of a residue at a position adjacent to but outside the MHC-binding site of the peptide. Further disclosed are the use of such modified peptides in treating, suppressing or preventing diseases such as infectious or allergic diseases and autoimmune diseases, in preventing or suppressing graft rejection, or in the eradication of tumor cells.

Abstract: The invention relates to methods of detecting the presence or absence of autoantibodies in an individual and to related methods and kits. In particular, the disclosure concerns measuring from one or more samples from an individual suspected of having a disease with an autoimmune component for binding of one or more autoantibodies to membrane vesicles comprising corresponding one or more antigens.

Abstract: The present invention provides modified natural killer T (NKT) cells, pharmaceutical compositions comprising the modified NKT cells and at least one pharmaceutically acceptable carrier or excipient, and uses of the modified NKT cells. Also disclosed herein are methods for enriching NKT cells and generating the modified natural killer T cells.

Abstract: Compositions that include one isolated, class I HLA-E trimolecular complex that includes a peptide ligand unique to M. tuberculosis-infected cells are disclosed. Isolated compositions that include the three components of the trimolecular complex and/or a polynucleotide encoding one or more of the three components are also disclosed.

Abstract: MICA and MICB are expressed on the surface of stressed, virus infected and cancer cells; they bind to their common receptor NKG2D on immune effector cells such as natural killer (NK) cells and some T cells to signal immune responses, including cytotoxicity, towards cells expressing surface MICA or MICB. To evade this immune-surveillance, virus infected cells and cancer cells shed the extracellular domain of their MICA and MICB as soluble forms (sMICA and sMICB) which act as decoys by binding and down-regulating expression of NKG2D on the immune effector cells. Antibodies are provided that specifically bind the soluble forms of both MICA and MICB to inhibit their adverse effects, but do not bind cell- or membrane-bound MICA and MICB to preserve their beneficial immune effects.

Abstract: The methods, compositions, and assays described herein are based, in part, on the discovery that CD1a mediates inflammation related to certain conditions such as urushiol exposure, psoriasis and other inflammatory skin diseases. One aspect provided herein relates to a method for treating or preventing an inflammatory skin disease, the method comprising: administering a therapeutically effective amount of an inhibitor of CD 1a to a subject having an inflammatory skin disease, thereby treating or preventing the inflammatory skin diseases.

Abstract: Methods of treating autoimmune diseases, such as vitiligo, by using compositions comprising DNA encoding a variant inducible heat shock protein 70 (HSP70i) having a mutation in the dendritic cell binding region thereof (HSP70i435-447) or an isolated variant gene product in the form of HSP70i with a modification in the dendritic cell activating region thereof (HSP70i435-447).

Abstract: Disclosed herein are modified NK cells, compositions comprising modified NK cells, and methods for treating a tumor or hyperproliferative disease in a subject. In some embodiments, the modified NK cells include NK cells including a heterologous nucleic acid molecule encoding a CD16 protein comprising a valine at amino acid position 158 (CD16-V158), a heterologous nucleic acid molecule encoding a CCR7 protein, or both. In some embodiments, methods include treating a subject with a tumor by administering a composition comprising an anti-cancer monoclonal antibody and administering a composition comprising the modified NK cells to the subject. Also disclosed are methods of making modified NK cells by obtaining a population of NK cells from a subject and transfecting the population of NK cells with a heterologous nucleic acid molecule encoding CD16-V158, a heterologous nucleic acid molecule encoding a CCR7 protein, or both.

Abstract: The present invention provides an agent for an immunocyte therapy, comprising an NKT cell obtained by differentiating in vitro a cell having the ?-chain region of the T cell receptor gene rearranged to uniform V?-J? in an NKT cell receptor-specific way, wherein an administration subject is an allogenic individual having MHC gene loci including at least one locus having a genotype different from that of the NKT cell. In addition, the present invention provides a bank of a human cell or an NKT cell derived from said cell, wherein the ?-chain region of a T cell receptor (TCR) gene has been rearranged to uniform V?-J?. The agent and cell bank of the present invention are useful for the prophylaxis and/or treatment of cancer, infection, an allergic disease or an autoimmune disease.

Abstract: Provided herein are compositions comprising anti-HLA-Ib antibodies (monoclonal, mixed monoclonal, recombinant, chimeric, humanized or human antibodies) as IVIg mimetics and methods for using the same for the prevention, treatment, therapy and/or amelioration of inflammation induced diseases and allograft rejection. In certain embodiments, the anti-HLA-Ib antibodies strongly mimic IVIg in immunoreactivity to HLA class Ia (HLA-A, HLA-B and HLA-Cw) and Ib antigens (HLA-E, HLA-F and HLA-G). In certain embodiments, the anti-HLA-Ib antibodies strongly mimic IVIg in immunomodulatory or immunosuppressive activities. Methods are also provided herein to induce production of polyclonal anti-HLA-Ib antibodies in cancer patients for restoring anti-tumor activities of CD8+ T cells and NK cells, by active specific immunotherapy.

Abstract: Materials and methods for identifying and using MEW molecule variants for activating self-reactive T cells in a peptide-specific manner, and their use to focus autoimmune cellular responses against diseases such as cancers and persisting viral infections, are described.