It is well known that CD4+ T cells consist of multiple functional subsets upon encountering antigens and these subsets regulate T cell responses against different antigens in different and complex environments. Th1 cells, for example, secrete IFN-��, IL-2, and GM-CSF; they actively regulate T cell proliferation, functional maturation of CD8+ T cells, and activation of several innate immune cell components, including myeloid dendritic cells, macrophages, and granulocytes. Th1 is pathogenic in multiple human autoimmune diseases and in T0070907 experimental models for EAE and CIA. Th2 cells distinguish themselves from other T cell subsets by secreting IL-4, IL-5, and IL-13; they actively promote IgE antibody production and regulate the immune response to allergens, including those involved in asthma and parasitic infections. Under the influence of IL-6, IL-21, and TGF-��, Th17 cells produces IL-17, and Th17 subsets regulate several autoimmune diseases, including EAE and CIA. The differentiation of Th cells Ropivacaine hydrochloride appears to be controlled at the transcriptional level: T-bet is critical for generating Th1 cells; GATA largely regulates Th2; ROR��t is a master transcription regulator for Th17.To delineate the role of B7-H3 in the differential regulation of T cell subsets, we constructed a B7-H3-deficient mouse strain and studied the differential roles of B7-H3 in these T cell subsets and in multiple mouse models where pathogenic T cells are biased toward specific T cell subsets. The effect of B7-H3 on the regulation of T cell responses has been evaluated in invitro cell culture systems and various murine models using transfection to overexpress B7-H3 monoclonal antibodies against B7-H3 and B7-H3 KO mice. These studies resulted in inconsistent and conflicting results from different laboratories. Invitro studies using human recombinant B7-H3 showed enhanced T cell growth in the presence of TCR engagement, which led to the hypothesis that B7-H3 is a costimulatory molecule for T cell growth. Using transfection to overexpress B7-H3 on cancer cells, researchers enhanced immune responses, especially in CD8+Tcell compartments; this was demonstrated by several investigators. Therefore, B7-H3 over-expression seemed costimulatory in T cell responses.