Th22 cells are an important source of IL-22 for host protection against enteropathogenic bacteria.
Th22 cells are an important source of IL-22 for host protection against enteropathogenic bacteria.
复制标题
DOI：
10.1016/j.immuni.2012.08.024
复制
发表时间：
2012-12-14
期刊：
影响因子：
32.4
通讯作者：
Weaver CT
中科院分区：
文献类型：
--
作者：
Basu R;O'Quinn DB;Silberger DJ;Schoeb TR;Fouser L;Ouyang W;Hatton RD;Weaver CT
白细胞介素-22（IL-22）是保护宿主免受屏障部位细菌感染的核心。先天性淋巴样细胞（ILC）和T细胞都产生IL-22。然而，CD 4 + T细胞的具体贡献及其发育起源尚不清楚。我们发现，肠道病原体啮齿柠檬酸杆菌诱导IL-22产生ILC和CD 4 + T细胞的连续波，这些细胞在原发感染期间对宿主防御至关重要。尽管ILC产生IL-22是严格依赖于IL-23的，但产生IL-22的CD 4 + T细胞的发育是通过IL-6依赖性机制发生的，该机制被IL-23增强但不依赖于IL-23，并且依赖于转录因子T-bet和AhR。在不存在TGF-β的情况下转移用IL-6分化的CD 4 + T细胞（“Th 22”细胞）赋予了对感染的IL-22缺陷小鼠的保护，而转移的Thl 7细胞则没有。这些发现确立了Th 22细胞作为粘膜抗微生物宿主防御的重要组分。
Interleukin-22 (IL-22) is central to host protection against bacterial infections at barrier sites. Both innate lymphoid cells (ILCs) and T cells produce IL-22. However, the specific contributions of CD4+ T cells and their developmental origins are unclear. We found that the enteric pathogen Citrobacter rodentium induced sequential waves of IL-22 producing ILCs and CD4+ T cells that were each critical to host defense during a primary infection. Whereas IL-22 production by ILCs was strictly IL-23–dependent, development of IL-22 producing CD4+ T cells occurred via an IL-6–dependent mechanism that was augmented by, but not dependent on, IL-23, and was dependent on both transcription factors T-bet and AhR. Transfer of CD4+ T cells differentiated with IL-6 in the absence of TGF-β (“Th22” cells) conferred protection of infected IL-22-deficient mice whereas transferred Th17 cells did not. These findings establish Th22 cells as an important component of mucosal anti-microbial host defense.
登录
查看更多内容
影响因子：
64.8
作者：
Cella, Marina;Fuchs, Anja;Vermi, William;Facchetti, Fabio;Otero, Karel;Lennerz, Jochen K. M.;Doherty, Jason M.;Mills, Jason C.;Colonna, Marco
通讯作者：
Colonna, Marco
影响因子：
30.5
作者：
Duhen, Thomas;Geiger, Rebekka;Sallusto, Federica
通讯作者：
Sallusto, Federica
影响因子：
64.8
作者：
通讯作者：
--
影响因子：
29.4
作者：
Andoh, A;Zhang, ZB;Fujiyama, Y
通讯作者：
Fujiyama, Y
DOI：
10.1038/nri2433
发表时间：
2008-11
期刊：
Nature reviews. Immunology
影响因子：
--
作者：
通讯作者：
--