Yang D D, Conze D, Whitmarsh A J, Barrett T, Davis R J, Rincón M, Flavell R A
Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA.
Immunity. 1998 Oct;9(4):575-85. doi: 10.1016/s1074-7613(00)80640-8.
Precursor CD4+ T cells develop into effector Th1 and Th2 cells that play a central role in the immune response. We show that the JNK MAP kinase pathway is induced in Th1 but not in Th2 effector cells upon antigen stimulation. Further, the differentiation of precursor CD4+ T cells into effector Th1 but not Th2 cells is impaired in JNK2-deficient mice. The inability of IL-12 to differentiate JNK2-deficient CD4+ T cells fully into effector Th1 cells is caused by a defect in IFNgamma production during the early stages of differentiation. The addition of exogenous IFNgamma during differentiation restores IL-12-mediated Th1 polarization in the JNK2-deficient mice. The JNK MAP kinase signaling pathway, therefore, plays an important role in the balance of Th1 and Th2 immune responses.
前体CD4 + T细胞发育成效应Th1和Th2细胞，它们在免疫反应中起核心作用。我们发现，抗原刺激后，JNK丝裂原活化蛋白激酶途径在Th1效应细胞中被诱导，但在Th2效应细胞中未被诱导。此外，在JNK2缺陷小鼠中，前体CD4 + T细胞向效应Th1细胞而非Th2细胞的分化受损。IL-12无法将JNK2缺陷的CD4 + T细胞完全分化为效应Th1细胞，这是由于分化早期IFNγ产生缺陷所致。在分化过程中添加外源性IFNγ可恢复JNK2缺陷小鼠中IL-12介导的Th1极化。因此，JNK丝裂原活化蛋白激酶信号通路在Th1和Th2免疫反应的平衡中起重要作用。
