Role of Schnurri-3 for immune response

SchNurri-3(shn-3)是Th2分化早期的重要分子，通过AP-1调节IL-4的产生。经抗原免疫后，T细胞特异性shn-3条件性基因敲除(shn-3 TKO)小鼠的IgE产量低于免疫对照小鼠。此外，当在促进Th17分化的条件下培养CD4+CD62L+初始T细胞时，shn-3缺陷的CD4+T细胞分化为Th17表型的频率高于对照CD4+T细胞。此外，Shn-3-TKO小鼠表现出T细胞介导的自身免疫性疾病EAE的发展和进展的强烈加剧。这些数据表明，SchNurri-3在免疫应答过程中决定辅助性T细胞的表型方面起着重要作用。

Schnurri-3 (Shn-3) is an essential molecule for the early stage of Th2 differentiation for regulation of IL-4 production by AP-1. Upon immunization with antigen, T cell-specific Shn-3 conditional knockout (Shn-3 TKO) mice had low IgE production compared to immunized control mice. Moreover, when CD4+CD62L+ naive T cells were cultured under condition to promote Th17 differentiation, Shn-3-deficient CD4+T cells differentiated to a Th17 phenotype more frequently than control CD4+T cells. Furthermore, Shn-3-TKO mice exhibited intense exacerbation of development and progression of T cell-mediated autoimmune disease EAE. These data suggest that Schnurri-3 plays an important role in determining the phenotype of helper T cells during an immunoresponse.