| First Author | Drujont L | Year | 2016 |
| Journal | Sci Rep | Volume | 6 |
| Pages | 23682 | PubMed ID | 27009467 |
| Mgi Jnum | J:251463 | Mgi Id | MGI:6102322 |
| Doi | 10.1038/srep23682 | Citation | Drujont L, et al. (2016) RORgammat+ cells selectively express redundant cation channels linked to the Golgi apparatus. Sci Rep 6:23682 |
| abstractText | Retinoid-related orphan receptor gamma t (RORgammat) 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 gammadelta T cells. Here we show that the intracellular ion channel TMEM176B and its homologue TMEM176A are strongly expressed in these RORgammat(+) 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 RORgammat(+) cells and indicate that both homologues should be simultaneously targeted to clearly elucidate the role of this intracellular ion flow. |
