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微生物如何打破白细胞介素-12家族成员之间的平衡。

How microorganisms tip the balance between interleukin-12 family members.

作者信息

Goriely Stanislas, Neurath Markus F, Goldman Michel

机构信息

Stanislas Goriely and Michel Goldman are at the Institute for Medical Immunology, Université Libre de Bruxelles, 8 rue Adrienne Bolland, B-6041 Charleroi, Belgium.

出版信息

Nat Rev Immunol. 2008 Jan;8(1):81-6. doi: 10.1038/nri2225.

Abstract

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.

摘要

白细胞介素-12p70(IL-12p70)可诱导辅助性T细胞1型(Th1)细胞应答,而相关细胞因子白细胞介素-23(IL-23)则是多种T细胞介导的炎症性疾病的主要开关。IL-12家族的另一个成员IL-27可调节先天性和适应性免疫应答。最近研究表明,不同组合的转录因子可调节编码这三种细胞因子的基因表达。Toll样受体配体与其他微生物产物和内源性介质共同作用,可打破IL-12家族成员表达之间的平衡,从而可能控制T细胞介导的炎症反应结果。在此基础上,我们提出了关于炎症性疾病发病机制和调控的新观点。

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