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RORγt+ cells selectively express redundant cation channels linked to the Golgi apparatus

Abstract : Retinoid-related orphan receptor gamma t (RORγt) is a master transcription factor central to type 17 immunity involving cells such as T helper 17, group 3 innate lymphoid cells or IL-17-producing γδ T cells. Here we show that the intracellular ion channel TMEM176B and its homologue TMEM176A are strongly expressed in these RORγt + cells. We demonstrate that TMEM176A and B exhibit a similar cation channel activity and mainly colocalise in close proximity to the trans-Golgi network. Strikingly, in the mouse, the loss of Tmem176b is systematically associated with a strong upregulation of Tmem176a. While Tmem176b single-deficiency has no effect on the course of experimental autoimmune encephalomyelitis, T cell or DSS-induced colitis, it significantly reduces imiquimod-induced psoriasis-like skin inflammation. These findings shed light on a potentially novel specific process linked to post-Golgi trafficking for modulating the function of RORγt + cells and indicate that both homologues should be simultaneously targeted to clearly elucidate the role of this intracellular ion flow.
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Lucile Drujont, Aurélie Lemoine, Aurélie Moreau, Géraldine Bienvenu, Mélanie Lancien, et al.. RORγt+ cells selectively express redundant cation channels linked to the Golgi apparatus. Scientific Reports, Nature Publishing Group, 2016, 6 (1), pp.23682. ⟨10.1038/srep23682⟩. ⟨inserm-02150842⟩



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