How microorganisms tip the balance between interleukin-12 family members
How microorganisms tip the balance between interleukin-12 family members
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DOI：
10.1038/nri2225
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发表时间：
2008-01-01
影响因子：
100.3
通讯作者：
Goldman, Michel
中科院分区：
文献类型：
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作者：
Goriely, Stanislas;Neurath, Markus F.;Goldman, Michel
白介素12p70(IL-12p70)诱导T辅助细胞反应，IL-23是相关细胞因子，是T细胞介导的炎症性疾病的主开关。IL-27是IL-12家族的另一个成员，调节先天和获得性免疫反应。最近，转录因子的不同组合被证明可以调节编码这三种细胞因子的基因的表达。Toll样受体配体与其他微生物产物和内源性介质共同改变IL-12家族成员的表达平衡，从而可能控制T细胞介导的炎症转归。在此基础上，我们对炎性疾病的发病机制和调控提出了一个新的视角。
Interleukin-12p70 (IL-12p70) induces T-helper-1-cell responses and IL-23, a related cytokine, is the master switch in several T-cell-mediated inflammatory disorders. IL-27, another member of the IL-12 family, regulates innate and adaptive immune responses. Recently, distinct combinations of transcription factors have been shown to regulate the expression of the genes that encode these three cytokines. Toll-like receptor ligands, in association with other microbial products and endogenous mediators, tip the balance between the expression of IL-12 family members and thereby may control the outcome of T-cell-mediated inflammation. On this basis, we present a novel perspective on the pathogenesis and regulation of inflammatory disorders.