Regulation of defense responses against protozoan infection by interleukin-27 and related cytokines.
Regulation of defense responses against protozoan infection by interleukin-27 and related cytokines.
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DOI：
10.1155/2007/79401
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发表时间：
2007
影响因子：
--
通讯作者：
Hamano S
中科院分区：
文献类型：
--
作者：
Yoshida H;Miyazaki Y;Wang S;Hamano S
细胞因子介导的免疫在抵御病原体方面至关重要。最近发现了IL-23和IL-27，它们与IL-12一起属于IL-12细胞因子家族。IL-27在诱导辅助性T细胞(Th)1应答中起关键作用，而IL-23在记忆型Th1细胞的增殖中起重要作用。最近的研究表明，IL-27也具有抗炎作用。在一些原虫感染中，各种促炎细胞因子过度产生，导致IL-27受体缺陷小鼠的致死性炎症反应。IL-27的抗炎作用至少部分依赖于抑制Th17细胞的发育，Th17细胞是一种新发现的Th细胞，由IL-23诱导，其特征是产生致炎细胞因子IL-17。因此，IL-27既是免疫反应的启动者，又是免疫反应和炎症的衰减剂。随着新的IL-12相关细胞因子和Th17细胞的发现，Th的发育正面临着一个新的范式。
Cytokine-mediated immunity is crucial in the defense against pathogens. Recently, IL-23 and IL-27 were identified, which along with IL-12 belong to the IL-12 cytokine family. IL-27 is pivotal for the induction of helper T cell (Th) 1 responses while IL-23 is important for the proliferation of memory type Th1 cells. Recent studies revealed that IL-27 also has an anti-inflammatory property. In some protozoan infection, various proinflammatory cytokines were over produced causing lethal inflammatory responses in IL-27 receptor-deficient mice. The anti-inflammatory effect of IL-27 depends, at least partly, on inhibition of the development of Th17 cells, a newly identified Th population that is induced by IL-23 and is characterized by the production of the inflammatogenic cytokine, IL-17. IL-27 thus has a double identity as an initiator and as an attenuator of immune responses and inflammation. With the discoveries of the new IL-12-related cytokines and Th17 cells, Th development is facing a new paradigm.
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影响因子：
64.8
作者：
Bettelli, E;Carrier, YJ;Kuchroo, VK
通讯作者：
Kuchroo, VK
影响因子：
32.4
作者：
Hamano, S;Himeno, K;Yoshida, H
通讯作者：
Yoshida, H
影响因子：
4.4
作者：
Bancroft, AJ;Humphreys, NE;Grencis, RK
通讯作者：
Grencis, RK
DOI：
10.1073/pnas.2536517100
发表时间：
2003-12-09
影响因子：
11.1
作者：
Lucas, S;Ghilardi, N;de Sauvage, FJ
通讯作者：
de Sauvage, FJ
影响因子：
64.8
作者：
Chen, Q;Ghilardi, N;de Sauvage, FJ
通讯作者：
de Sauvage, FJ