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Microbiota-induced tissue signals regulate ILC3-mediated antigen presentation
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Journal Article
Microbiota-induced tissue signals regulate ILC3-mediated antigen presentation
2020
Overview
Although group 3 innate lymphoid cells (ILC3s) are efficient inducers of T cell responses in the spleen, they fail to induce CD4
+
T cell proliferation in the gut. The signals regulating ILC3-T cell responses remain unknown. Here, we show that transcripts associated with MHC II antigen presentation are down-modulated in intestinal natural cytotoxicity receptor (NCR)
−
ILC3s. Further data implicate microbiota-induced IL-23 as a crucial signal for reversible silencing of MHC II in ILC3s, thereby reducing the capacity of ILC3s to present antigen to T cells in the intestinal mucosa. Moreover, IL-23-mediated MHC II suppression is dependent on mTORC1 and STAT3 phosphorylation in NCR
−
ILC3s. By contrast, splenic interferon-γ induces MHC II expression and CD4
+
T cell stimulation by NCR
−
ILC3s. Our results thus identify biological circuits for tissue-specific regulation of ILC3-dependent T cell responses. These pathways may have implications for inducing or silencing T cell responses in human diseases.
Group 3 innate lymphoid cells (ILC3s) promote T cell activation in the spleen but suppress it in the gut. Here, the authors show that this distinct regulation is mediated by gut microbiota-induced IL-23 and IFN-γ, respectively, and, along with the article by Rao et al, this work elucidates how cytokines set context specificity of ILC-T cell crosstalk by regulating ILC antigen presentation.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 13/31
/ 38/88
/ 38/91
/ 64/110
/ 64/60
/ Animals
/ Antigen Presentation - immunology
/ Antigen-Presenting Cells - cytology
/ Antigen-Presenting Cells - immunology
/ Antigens
/ Histocompatibility Antigens Class II - metabolism
/ Humanities and Social Sciences
/ Interferon-gamma - metabolism
/ Lymphocyte Activation - immunology
/ Major histocompatibility complex
/ Mechanistic Target of Rapamycin Complex 1 - metabolism
/ Mice
/ Mucosa
/ Nuclear Proteins - metabolism
/ Principal Component Analysis
/ Promoter Regions, Genetic - genetics
/ Science
/ Spleen
/ STAT3 Transcription Factor - metabolism
/ Toxicity
