Abstract: Abstract: The present disclosure is directed to fusion proteins comprising a Tumor Necrosis Factor ? (TNF?) binding protein and an interleukin-10 (IL-10) molecule, methods of making the fusion proteins, and methods of treating or preventing autoimmune and inflammatory conditions using the fusion proteins.

Abstract: The disclosure provides methods for the selection and isolation of T cells expressing programmed cell death 1 (PD-1) and for selecting a PD-1 expression level of the isolated PD-1 expressing T cells. The disclosure also provides methods of large scale expansion of selected and isolated PD-1 expressing T cells, as well as methods for treating a subject comprising administering selected and isolated PD-1 expressing T cells to the subject.

Abstract: Described herein are methods and compositions for treating autoimmunity and inflammatory conditions without non-specific suppression of the host immune system. In particular, the anti-OX40L antibodies described herein are unique in that they not only inhibit the differentiation of inflammatory T cells but also promote the generation and function of regulatory T cells by inducing IL-10 and inhibiting TNF-? and by reducing aberrant Th2 cell responses. Furthermore, the methods and compositions described herein eliminate or reduce aberrant T follicular helper cell—(Tfh) responses that may contribute to the pathogenicity of autoimmune disease.

Abstract: Described herein are methods and compositions for treating autoimmunity and inflammatory conditions without non-specific suppression of the host immune system. In particular, the anti-OX40L antibodies described herein are unique in that they not only inhibit the differentiation of inflammatory T cells but also promote the generation and function of regulatory T cells by inducing IL-10 and inhibiting TNF-? and by reducing aberrant Th2 cell responses. Furthermore, the methods and compositions described herein eliminate or reduce aberrant T follicular helper cell—(Tfh) responses that may contribute to the pathogenicity of autoimmune disease.

Abstract: Described herein are methods and compositions for treating autoimmunity and inflammatory conditions without non-specific suppression of the host immune system. In particular, the anti-OX40L antibodies described herein are unique in that they not only inhibit the differentiation of inflammatory T cells but also promote the generation and function of regulatory T cells by inducing IL-10 and inhibiting TNF-? and by reducing aberrant Th2 cell responses. Furthermore, the methods and compositions described herein eliminate or reduce aberrant T follicular helper cell—(Tfh) responses that may contribute to the pathogenicity of autoimmune disease.

Abstract: Described herein are methods and compositions for treating autoimmunity and inflammatory conditions without non-specific suppression of the host immune system. In particular, the anti-OX40L antibodies described herein are unique in that they not only inhibit the differentiation of inflammatory T cells but also promote the generation and function of regulatory T cells by inducing IL-10 and inhibiting TNF-? and by reducing aberrant Th2 cell responses. Furthermore, the methods and compositions described herein eliminate or reduce aberrant T follicular helper cell- (Tfh) responses that may contribute to the pathogenicity of autoimmune disease.

Abstract: Provided are methods of modulating activity of regulatory T cells, CD4+ T cells, and CD8+ T cells. Also provided are methods of treating immune disorders.

Abstract: Provided are methods of modulating activity of regulatory T cells, CD4+ T cells, and CD8+ T cells. Also provided are methods of treating immune disorders.

Abstract: The present invention provides a immunogenic composition for inducing an immune response containing a CTL recognition antigen or an antigen epitope thereof, which can be obtained by screening a CTL recognition antigen or an antigen epitope thereof having an anti-tumor effect against HTLV-I tumors such as ATL, or a DNA that encodes them as an active ingredient and the like. Dominant epitope GAFLTNVPY was identified by the following steps: splenic T cells derived from immunocompetent rats immunized with HTLV-I-infected cell lines were stimulated with formalin-fixed HTLV-I-infected cell lines; HTLV-I-specific CTL cell lines were established; cytotoxic activities of the above-mentioned HTLV-I-specific CTL cell lines against target cells G14 sensitized with synthetic peptides which are candidate for an epitope were measured.