TNF superfamily member TL1A elicits type 2 innate lymphoid cells at mucosal barriers

被引：137

作者：

Yu, X. ^{[1
]}

Pappu, R. ^{[1
]}

Ramirez-Carrozzi, V. ^{[1
]}

Ota, N. ^{[1
]}

Caplazi, P. ^{[2
]}

Zhang, J. ^{[3
]}

Yan, D. ^{[3
]}

Xu, M. ^{[3
]}

Lee, W. P. ^{[3
]}

Grogan, J. L. ^{[1
]}

机构：

[1] Genentech Inc, Dept Immunol, San Francisco, CA 94080 USA

[2] Genentech Inc, Dept Pathol, San Francisco, CA 94080 USA

[3] Genentech Inc, Dept Translat Immunol, San Francisco, CA 94080 USA

来源：

MUCOSAL IMMUNOLOGY | 2014年 / 7卷 / 03期

关键词：

TRANSCRIPTION FACTOR GATA3; SUSCEPTIBILITY; EXPRESSION; CYTOKINES; EFFECTOR; POPULATION; RESPONSES; LIGAND; IL-13; DR3;

D O I：

10.1038/mi.2013.92

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Immune responses at mucosal barriers are regulated by innate type 2 lymphoid cells (ILC2s) that elaborate effector cytokines interleukins 5 and 13 (IL5 and IL13). IL25 and IL33 are key cytokines that support ILC2s; however, mice deficient in these pathways retain some functional ILC2s. Analysis of human and murine cells revealed that ILC2s highly express tumor necrosis factor (TNF)-receptor superfamily member DR3 (TNFRSF25). Engagement of DR3 with cognate ligand TL1A promoted ILC2 expansion, survival, and function. Exogenous protein or genetic overexpression of TL1A activated ILC2s independent of IL25 or IL33.Dr3(-/-) mice failed to control gut helminthic infections, and failed to mount ILC2 responses in the lung after nasal challenge with papain. Our data demonstrate a key role for TL1A in promoting ILC2s at mucosal barriers.

引用

页码：730 / 740

页数：11

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