Innate lymphoid cells promote anatomical containment of lymphoid-resident commensal bacteria.
Innate lymphoid cells promote anatomical containment of lymphoid-resident commensal bacteria.
复制标题
DOI：
10.1126/science.1222551
复制
发表时间：
2012-06-08
期刊：
影响因子：
--
通讯作者：
Artis D
中科院分区：
文献类型：
--
作者：
Sonnenberg GF;Monticelli LA;Alenghat T;Fung TC;Hutnick NA;Kunisawa J;Shibata N;Grunberg S;Sinha R;Zahm AM;Tardif MR;Sathaliyawala T;Kubota M;Farber DL;Collman RG;Shaked A;Fouser LA;Weiner DB;Tessier PA;Friedman JR;Kiyono H;Bushman FD;Chang KM;Artis D
哺乳动物的肠道被数以万亿计的有益肠道细菌定殖，这些细菌在解剖学上被限制在特定的小生境中。然而，调节解剖包容性的机制仍不清楚。在这里，我们确定，白细胞介素（IL）-22产生先天淋巴细胞（ILC）存在于肠道组织的健康哺乳动物。ILC的消耗导致肠道细菌的外周传播和全身性炎症，这通过施用IL-22来预防。传播细菌被鉴定为源自宿主淋巴组织的产碱菌属。在小鼠中，产碱菌足以促进ILC耗竭后的全身炎症，并且产碱菌特异性全身免疫应答与患者中的克罗恩病和进行性HCV感染相关。总的来说，这些数据表明，ILC调节淋巴驻留细菌的选择性遏制，以防止与慢性疾病相关的全身炎症。
The mammalian intestinal tract is colonized by trillions of beneficial commensal bacteria that are anatomically restricted to specific niches. However, the mechanisms that regulate anatomical containment remain unclear. Here we identify that interleukin (IL)-22-producing innate lymphoid cells (ILCs) are present in intestinal tissues of healthy mammals. Depletion of ILCs resulted in peripheral dissemination of commensal bacteria and systemic inflammation, which was prevented by administration of IL-22. Disseminating bacteria were identified as Alcaligenes species originating from host lymphoid tissues. Alcaligenes was sufficient to promote systemic inflammation following ILC-depletion in mice, and Alcaligenes-specific systemic immune responses were associated with Crohn's disease and progressive HCV infection in patients. Collectively, these data indicate that ILCs regulate selective containment of lymphoid-resident bacteria to prevent systemic inflammation associated with chronic diseases.
登录
查看更多内容
影响因子：
6.7
作者：
Bergstrom KS;Kissoon-Singh V;Gibson DL;Ma C;Montero M;Sham HP;Ryz N;Huang T;Velcich A;Finlay BB;Chadee K;Vallance BA
通讯作者：
Vallance BA
影响因子：
32.4
作者：
Sonnenberg GF;Monticelli LA;Elloso MM;Fouser LA;Artis D
通讯作者：
Artis D
影响因子：
25.7
作者：
Parlesak, A;Schäfer, C;Bode, C
通讯作者：
Bode, C
影响因子：
82.9
作者：
Zheng, Yan;Valdez, Patricia A.;Ouyang, Wenjun
通讯作者：
Ouyang, Wenjun
先天和适应性免疫会灵活合作，以维持宿主 - 微生物互助。
DOI：
10.1126/science.1172747
发表时间：
2009-07-31
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Slack E;Hapfelmeier S;Stecher B;Velykoredko Y;Stoel M;Lawson MA;Geuking MB;Beutler B;Tedder TF;Hardt WD;Bercik P;Verdu EF;McCoy KD;Macpherson AJ
通讯作者：
Macpherson AJ