Evidence map›Paper›PMID 27009467›Full record

ArticleScientific reports2016

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

Lucile Drujont, Aurélie Lemoine, Aurélie Moreau, Géraldine Bienvenu, Mélanie Lancien, Thierry Cens, Flora Guillot, Gaëlle Bériou, Laurence Bouchet-Delbos, Hans Jörg Fehling and 7 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.4field-weighted citation impact, top 19% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

28 citing papers in PubMed, 54 citations in OpenAlex.

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  15. Isotype-specific plasma cells express divergent transcriptional programs.Proceedings of the National Academy of Sciences of the United States of America · 2022
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  20. The intracellular cation channel TMEM176B as a dual immunoregulator.Frontiers in cell and developmental biology · 2022
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

17 authors at 5 institutions in 1 country.

Lucile DrujontINSERM UMR 1064, Center for Research in Transplantation and Immunology; Université de Nantes; CHU Nantes, Institut de Transplantation Urologie Néphrologie (ITUN); 44093 Nantes, France.
Aurélie LemoineINSERM UMR 1064, Center for Research in Transplantation and Immunology; Université de Nantes; CHU Nantes, Institut de Transplantation Urologie Néphrologie (ITUN); 44093 Nantes, France.
Aurélie MoreauINSERM UMR 1064, Center for Research in Transplantation and Immunology; Université de Nantes; CHU Nantes, Institut de Transplantation Urologie Néphrologie (ITUN); 44093 Nantes, France.
Géraldine BienvenuINSERM UMR 1064, Center for Research in Transplantation and Immunology; Université de Nantes; CHU Nantes, Institut de Transplantation Urologie Néphrologie (ITUN); 44093 Nantes, France.
Mélanie LancienINSERM UMR 1064, Center for Research in Transplantation and Immunology; Université de Nantes; CHU Nantes, Institut de Transplantation Urologie Néphrologie (ITUN); 44093 Nantes, France.
Thierry CensCNRS UMR 5237, CRBM, 34293 Montpellier, France.
Flora GuillotINSERM UMR 1064, Center for Research in Transplantation and Immunology; Université de Nantes; CHU Nantes, Institut de Transplantation Urologie Néphrologie (ITUN); 44093 Nantes, France.
Gaëlle BériouINSERM UMR 1064, Center for Research in Transplantation and Immunology; Université de Nantes; CHU Nantes, Institut de Transplantation Urologie Néphrologie (ITUN); 44093 Nantes, France.
Laurence Bouchet-DelbosINSERM UMR 1064, Center for Research in Transplantation and Immunology; Université de Nantes; CHU Nantes, Institut de Transplantation Urologie Néphrologie (ITUN); 44093 Nantes, France.
Hans Jörg FehlingInstitute of Immunology, University Clinics Ulm, 8901 Ulm, Germany.
Elise ChiffoleauINSERM UMR 1064, Center for Research in Transplantation and Immunology; Université de Nantes; CHU Nantes, Institut de Transplantation Urologie Néphrologie (ITUN); 44093 Nantes, France.
Arnaud B NicotINSERM UMR 1064, Center for Research in Transplantation and Immunology; Université de Nantes; CHU Nantes, Institut de Transplantation Urologie Néphrologie (ITUN); 44093 Nantes, France.
Pierre CharnetCNRS UMR 5237, CRBM, 34293 Montpellier, France.
Jérôme C MartinINSERM UMR 1064, Center for Research in Transplantation and Immunology; Université de Nantes; CHU Nantes, Institut de Transplantation Urologie Néphrologie (ITUN); 44093 Nantes, France.
Régis JosienINSERM UMR 1064, Center for Research in Transplantation and Immunology; Université de Nantes; CHU Nantes, Institut de Transplantation Urologie Néphrologie (ITUN); 44093 Nantes, France.
Maria Cristina CuturiINSERM UMR 1064, Center for Research in Transplantation and Immunology; Université de Nantes; CHU Nantes, Institut de Transplantation Urologie Néphrologie (ITUN); 44093 Nantes, France.
Cédric LouvetINSERM UMR 1064, Center for Research in Transplantation and Immunology; Université de Nantes; CHU Nantes, Institut de Transplantation Urologie Néphrologie (ITUN); 44093 Nantes, France.
Institut de Transplantation Urologie en Nephrologie · FRInserm · FRNantes Université · FRCentre de Recherche en Biologie cellulaire de Montpellier · FRCentre National de la Recherche Scientifique · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

AnimalsCells, CulturedColitisDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalHumansMembrane ProteinsMiceNuclear Receptor Subfamily 1, Group F, Member 3PsoriasisT-Lymphocytes, Helper-Inducertrans-Golgi NetworkMembrane ProteinsNuclear Receptor Subfamily 1, Group F, Member 3TMEM176A protein, humanTmem176A protein, mouseTMEM176B protein, humanTmem176B protein, mouse

Identifiers

PMID27009467
PMCPMC4806298
OpenAlexW2331550775

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.