期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 214, 期 9, 页码 2507-2521出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20170051
关键词
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资金
- Science Foundation Ireland [10/IN.1/B3004]
- Wellcome Trust [092530/Z/10/Z]
- National Children's Research Centre
- Wellcome Trust [092530/Z/10/Z] Funding Source: Wellcome Trust
- MRC [MC_U105178805] Funding Source: UKRI
- Science Foundation Ireland (SFI) [10/IN.1/B3004] Funding Source: Science Foundation Ireland (SFI)
- Medical Research Council [MC_U105178805] Funding Source: researchfish
Group 2 innate lymphoid cells (ILC2s) are important effector cells driving the initiation of type 2 immune responses leading to adaptive T helper 2 (Th2) immunity. Here we show that ILC2s dynamically express the checkpoint inhibitor molecule PD-L1 during type 2 pulmonary responses. Surprisingly, PD-L1 : PD-1 interaction between ILC2s and CD4(+) T cells did not inhibit the T cell response, but PD-L1-expressing ILC2s stimulated increased expression of GATA3 and production of IL-13 by Th2 cells both in vitro and in vivo. Conditional deletion of PD-L1 on ILC2s impaired early Th2 polarization and cytokine production, leading to delayed worm expulsion during infection with the gastrointestinal helminth Nippostrongylus brasiliensis. Our results identify a novel PD-L1-controlled mechanism for type 2 polarization, with ILC2s mediating an innate checkpoint to control adaptive T helper responses, which has important implications for the treatment of type 2 inflammation.
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