The chemokine CCL6 promotes innate immunity via immune cell activation and recruitment
The chemokine CCL6 promotes innate immunity via immune cell activation and recruitment
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DOI：
10.4049/jimmunol.179.8.5474
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发表时间：
2007-10-15
影响因子：
4.4
通讯作者：
Kunkel, Steven L.
中科院分区：
文献类型：
--
作者：
Coelho, Ana L.;Schaller, Matthew A.;Kunkel, Steven L.
脓毒症是先天免疫功能衰竭的结果。最近的研究表明，CC趋化因子CCL6通过一种未知的机制增强了实验性败血症期间的抗菌免疫。本研究表明，转基因CCL6表达通过调节腹膜细胞活化，更重要的是通过将产生ifn的NK细胞和杀伤树突状细胞募集到腹膜中，从而消除败血性腹膜炎模型中的死亡率。因此，CCL6减轻败血症期间的免疫衰竭，部分是通过1型细胞因子介导的保护性机制。
Septic syndrome is a consequence of innate immune failure. Recent studies showed that the CC chemokine CCL6 enhanced antimicrobial immunity during experimental sepsis through an unknown mechanism. The present study demonstrates that transgenic CCL6 expression abolishes mortality in a septic peritonitis model via the modulation of resident peritoneal cell activation and, more importantly, through the recruitment of IFN-producing NK cells and killer dendritic cells into the peritoneum. Thus, CCL6 attenuates the immune failure during sepsis, in part, through a protective type 1-cytokine mediated mechanism.