Journal
SCIENTIFIC REPORTS
Volume 6, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/srep23682
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Funding
- Labex IGO project - Investissements d'Avenir French Government programme [ANR-11-LABX-0016-01]
- French government [ANR-10-IBHU-005]
- Nantes Metropole
- region Pays de la Loire
- Inserm-Region Pays de la Loire fellowship
- Fondation Progreffe
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Retinoid-related orphan receptor gamma t (ROR gamma t) 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 gamma delta T cells. Here we show that the intracellular ion channel TMEM176B and its homologue TMEM176A are strongly expressed in these ROR gamma t(+) 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 ROR gamma t(+) cells and indicate that both homologues should be simultaneously targeted to clearly elucidate the role of this intracellular ion flow.
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