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Leng, Tianqi; Akther, Hossain Delowar; Hackstein, Carl-Philipp; Powell, Kate; King, Thomas; Friedrich, Matthias; Christoforidou, Zoe; McCuaig, Sarah; Neyazi, Mastura; Arancibia-Cárcamo, Carolina V.; Hagel, Joachim; Powrie, Fiona; Peres, Raphael Sanches; Millar, Val; Ebner, Daniel; Lamichhane, Rajesh; Ussher, James; Hinks, Timothy S.C.; Marchi, Emanuele; Willberg, Chris; Klenerman, Paul
Cell reports (Cambridge), 09/2019, Volume: 28, Issue: 12Journal Article
MAIT cells are an unconventional T cell population that can be activated through both TCR-dependent and TCR-independent mechanisms. Here, we examined the impact of combinations of TCR-dependent and TCR-independent signals in human CD8+ MAIT cells. TCR-independent activation of these MAIT cells from blood and gut was maximized by extending the panel of cytokines to include TNF-superfamily member TL1A. RNA-seq experiments revealed that TCR-dependent and TCR-independent signals drive MAIT cells to exert overlapping and specific effector functions, affecting both host defense and tissue homeostasis. Although TCR triggering alone is insufficient to drive sustained activation, TCR-triggered MAIT cells showed specific enrichment of tissue-repair functions at the gene and protein levels and in in vitro assays. Altogether, these data indicate the blend of TCR-dependent and TCR-independent signaling to CD8+ MAIT cells may play a role in controlling the balance between healthy and pathological processes of tissue inflammation and repair. Display omitted •Activation of human MAIT cells is TCR-dependent or TCR-independent and enhanced by TL1A•TCR-dependent and TCR-independent triggering induces distinct transcriptional responses•TCR-dependent triggering of MAIT cells induces a tissue-repair program•Data integration with in vivo studies in mice indicates a shared transcriptome Leng et al. explore the consequences of activation of human MAIT cells via their TCR and/or cytokines, including the gut-associated TNF-superfamily member TL1A. TCR triggering reveals a transcriptional program linked to tissue-repair functions seen in vivo, consistent with a homeostatic role for these cells in epithelia.
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