IL-22 mediates mucosal host defense against Gram-negative bacterial pneumonia
IL-22 mediates mucosal host defense against Gram-negative bacterial pneumonia
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DOI：
10.1038/nm1710
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发表时间：
2008-03-01
期刊：
影响因子：
82.9
通讯作者：
Kolls, Jay K.
中科院分区：
文献类型：
--
作者：
Aujla, Shean J.;Chan, Yvonne R.;Kolls, Jay K.
新出现的证据支持T辅助细胞17型（T（H）17）细胞除了介导自身免疫外，在针对细胞外病原体的粘膜免疫中具有关键作用的概念。白细胞介素-22（IL-22）和IL-17 A都是由T（H）17谱系产生的效应细胞因子，并且都是维持革兰氏阴性肺病原体肺炎克雷伯氏菌局部控制的关键。虽然这两种细胞因子调节CXC趋化因子和粒细胞集落刺激因子在肺中的产生，但只有IL-22增加肺上皮细胞增殖和增加对损伤的跨上皮抗性。这些数据支持T（H）17细胞谱系及其效应分子已经进化以影响宿主在粘膜部位对细胞外病原体的防御的概念。
Emerging evidence supports the concept that T helper type 17 (T(H)17) cells, in addition to mediating autoimmunity, have key roles in mucosal immunity against extracellular pathogens. Interleukin-22 (IL-22) and IL-17A are both effector cytokines produced by the T(H)17 lineage, and both were crucial for maintaining local control of the Gram-negative pulmonary pathogen, Klebsiella pneumoniae. Although both cytokines regulated CXC chemokines and granulocyte colony-stimulating factor production in the lung, only IL-22 increased lung epithelial cell proliferation and increased transepithelial resistance to injury. These data support the concept that the T(H)17 cell lineage and its effector molecules have evolved to effect host defense against extracellular pathogens at mucosal sites.