MHCII-Mediated Dialog between Group 2 Innate Lymphoid Cells and CD4+ T Cells Potentiates Type 2 Immunity and Promotes Parasitic Helminth Expulsion

被引:670
作者
Oliphant, Christopher J. [1 ]
Hwang, You Yi [1 ]
Walker, Jennifer A. [1 ]
Salimi, Maryam [2 ]
Wong, See Heng [1 ]
Brewer, James M. [6 ]
Englezakis, Alexandros [1 ]
Barlow, Jillian L. [1 ]
Hams, Emily [3 ]
Scanlon, Seth T. [1 ]
Ogg, Graham S. [2 ]
Fallon, Padraic G. [3 ,4 ,5 ]
McKenzie, Andrew N. J. [1 ]
机构
[1] MRC, Mol Biol Lab, Cambridge CB2 0QH, England
[2] Univ Oxford, John Radcliffe Hosp, NIHR Biomed Res Ctr, MRC Human Immunol Unit, Oxford OX3 9DS, England
[3] Trinity Coll Dublin, Trinity Biomed Sci Inst, Dublin 2, Ireland
[4] Our Ladys Childrens Hosp, Natl Childrens Res Ctr, Dublin 12, Ireland
[5] Trinity Coll Dublin, Inst Mol Med, Dublin 2, Ireland
[6] Univ Pl, GRBC, Inst Infect Immun & Inflammat, Glasgow G12 8TA, Lanark, Scotland
基金
爱尔兰科学基金会; 英国惠康基金; 英国医学研究理事会;
关键词
CYSTEINE PROTEASE; TH2; IMMUNITY; IN-VIVO; IL-4; EXPRESSION; RESPONSES; INFLAMMATION; CONTRIBUTE; INDUCTION; CYTOKINES;
D O I
10.1016/j.immuni.2014.06.016
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
071005 [微生物学]; 100108 [医学免疫学];
摘要
Group 2 innate lymphoid cells (ILC2s) release interleukin-13 (IL-13) during protective immunity to helminth infection and detrimentally during allergy and asthma. Using two mouse models to deplete ILC2s in vivo, we demonstrate that T helper 2 (Th2) cell responses are impaired in the absence of ILC2s. We show that MHCII-expressing ILC2s interact with antigen-specific T cells to instigate a dialog in which IL-2 production from T cells promotes ILC2 proliferation and IL-13 production. Deletion of MHCII renders IL-13-expressing ILC2s incapable of efficiently inducing Nippostrongylus brasiliensis expulsion. Thus, during transition to adaptive T cell-mediated immunity, the ILC2 and T cell crosstalk contributes to their mutual maintenance, expansion and cytokine production. This interaction appears to augment dendritic-cell-induced T cell activation and identifies a previously unappreciated pathway in the regulation of type-2 immunity.
引用
收藏
页码:283 / 295
页数:13
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