Korn Thomas, Oukka Mohamed, Kuchroo Vijay, Bettelli Estelle
Center for Neurologic Diseases, Brigham & Women's Hospital, Harvard Medical School, 77 Avenue Louis Pasteur, HIM780, Boston, MA 02115, USA.
Semin Immunol. 2007 Dec;19(6):362-71. doi: 10.1016/j.smim.2007.10.007. Epub 2007 Nov 26.
Upon activation, naïve CD4(+) T cells differentiate into effector T cells with specific effector functions and cytokine profiles. The Th1/Th2 paradigm has recently been reevaluated to include a third population of T helper cells, producing IL-17 and designated Th17. The differentiation of Th17 cells requires the coordinate and specific action of the proinflammatory cytokine IL-6 and the immunosuppressive cytokine TGF-beta. In addition, the IL-12 family member IL-23 is involved in the maintenance of these cells. Analogous to other T helper cell subsets, Th17 commitment is initiated by sequential involvement of STAT molecules, i.e. STAT3 downstream of cytokine receptors, and specific transcription factors, i.e. ROR-gammat. Recent data also support the existence of a complex network of cytokines regulating Th17 cells. Clearly, the specific effector functions of Th17 cells expand beyond previously described effects of Th1 and Th2 immunity, with specific roles in host defense against certain pathogens and in organ-specific autoimmunity. The potential dynamics of Th17 cell populations and their interplay with other inflammatory cells in the induction of tissue inflammation in host defense and organ-specific autoimmunity are discussed.
激活后，初始CD4(+) T细胞分化为具有特定效应功能和细胞因子谱的效应T细胞。Th1/Th2模式最近被重新评估，纳入了第三种T辅助细胞群，即产生IL-17的Th17细胞。Th17细胞的分化需要促炎细胞因子IL-6和免疫抑制细胞因子TGF-β的协同和特异性作用。此外，IL-12家族成员IL-23参与这些细胞的维持。与其他T辅助细胞亚群类似，Th17细胞的定向分化由STAT分子（即细胞因子受体下游的STAT3）和特定转录因子（即ROR-γt）的顺序参与启动。最近的数据也支持存在一个调节Th17细胞的复杂细胞因子网络。显然，Th17细胞的特定效应功能超出了先前描述的Th1和Th2免疫效应，在宿主抵御某些病原体和器官特异性自身免疫中发挥特定作用。本文讨论了Th17细胞群体的潜在动态及其在宿主防御和器官特异性自身免疫中诱导组织炎症时与其他炎症细胞的相互作用。
