The present disclosure is directed recombinant T cell receptors capable of binding a tyrosinase epitope, a MAGA-A1 epitope, a MART1 epitope, a MAGE-A3 epitope, or an SSX2 epitope and nucleic acid molecules encoding the same. In some embodiments, the nucleic acid molecules further comprise a second nucleotide sequence, wherein the second nucleotide sequence or the polypeptide encoded by the second nucleotide sequence inhibits the expression of an endogenous TCR. Other aspects of the disclosure are directed to vectors comprising the nucleic acid molecule and cells comprising the recombinant TCR, the nucleic acid molecule, or the vector. Still other aspects of the disclosure are directed to methods of using the same. In some embodiments, the methods comprise treating a cancer in a subject in need thereof.

Provided herein are CD25 chimeric antigen receptors and compositions and methods for using the same. Methods for using CD25 chimeric antigen receptors provided herein include, for example, methods of treatment, methods of enhancing the immune system in a subject, and methods of killing a target cell or a population of target cells.

The present application relates to the field of RNA interference, more particularly RNA interference as applied in immunotherapy, such as adoptive cell therapy (ACT). Here, multiple shRNAs, designed to downregulate multiple targets are proposed. Also proposed are polynucleotides, vectors encoding the shRNA and cells expressing such shRNAs, alone or in combination with a protein of interest such as a chimeric antigen receptor (CAR) or T cell receptor (TCR). These cells are particularly suitable for use in immunotherapy.

Methods of preventing or treating autoimmune disease are disclosed. In some cases, subjects with having or at risk of developing autoimmune disease are identified as possessing one or more autoimmunity-susceptibility HLA alleles at one or more HLA loci. In many cases, the HLA loci are selected from Class I and Class II loci, for example Class I A, B, and C, and Class II DQ, DR, and DP. In many cases, subjects suffering from or at risk of developing an autoimmune disease may be administered a plurality engineered autologous HSCs modified to carry and express a variant susceptibility allele having at least one mutation in the antigen binding cleft that alters antigen binding and/or specificity of that variant HLA molecule. In many embodiments, the engineered HSCs are CD34+ immune cells that express one or more modified HLA proteins.

T cell receptors that recognize or bind to human papilloma virus (HPV) antigens, genetically engineered cells and cell-based therapies are provided.

The present disclosure provides methods for generating induced cardiomyocytes by expression of selected microRNAs with MYOCD and ASCL1, or with MYOCD alone. Illustrative microRNAs include miR-133, miR-1, miR-19, and/or miR-20b. The present disclosure further provides gene-delivery vectors comprising one or more polynucleotides encoding a selected microRNA with YOCD, withMYOCD and ASCL1, with MYOCD-2A-ASCL1, or with ASCL1-2A-MYOCD. It further provides methods of using such compositions and vectors, or induced cardiomyocytes generated with these factors, for treating a heart condition.

This invention is directed to, inter alia, stable cartilage-derived progenitor cell lines as well as methods for producing stable cartilage-derived progenitor cell lines from diseased human cartilaginous tissues and lesions. Also provided herein are methods for using cartilage-derived progenitor cell lines for treatment of cartilage and bone degenerative diseases.

Provided herein are compositions and methods for adoptive cell therapy comprising engineered immune cells that express an antigen-targeted chimeric antigen receptor and a prodrug converting enzyme for the treatment of inflammation, inflammatory diseases, or pathogenic infections.

The present invention provides compositions and methods for immunotherapy in human. The invention includes a B cell receptor like complex expressed in T cells and comprising an extracellular antigen recognition domain, a trans-membrane domain, a CD79αβ heterodimer, and a signaling region that controls T cell activation. The extracellular antigen recognition domain and trans-membrane are derived from the same human or humanized B cell receptor and form a single unit in the complex. The signaling region comprises a T cell signaling domain in combination with a co-stimulatory signaling domain. The signaling region is fused to the CD79αβ heterodimer. Furthermore, the B cell receptor like complex of the present invention can use a targeting molecule as a bridge between cytotoxic T cells and targeted cells.

Methods of preventing or treating autoimmune disease are disclosed. In some cases, subjects with having or at risk of developing autoimmune disease are identified as possessing one or more autoimmunity-susceptibility HLA alleles at one or more HLA loci. In many cases, the HLA loci are selected from Class I and Class II loci, for example Class I A, B, and C, and Class II DQ, DR, and DP. In many cases, subjects suffering from or at risk of developing an autoimmune disease may be administered a plurality engineered autologous HSCs modified to carry and express a variant susceptibility allele having at least one mutation in the antigen binding cleft that alters antigen binding and/or specificity of that variant HLA molecule. In many embodiments, the engineered HSCs are CD34+ immune cells that express one or more modified HLA proteins.