Evidence map›Paper›PMID 35020849›Full record

ArticleClinical and experimental immunology2022

RORγt+Foxp3+ regulatory T cells in the regulation of autoimmune arthritis.

Kotona Furuyama, Yuya Kondo, Masaru Shimizu, Masahiro Yokosawa, Seiji Segawa, Akira Iizuka, Reona Tanimura, Hiroto Tsuboi, Isao Matsumoto, Takayuki Sumida

Open access · bronzeAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

11 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
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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

10 authors at 1 institution in 1 country.

Kotona FuruyamaDepartment of Internal Medicine, Faculty of Medicine, University of Tsukuba, Tsukuba City, Ibaraki, Japan.
Yuya KondoDepartment of Internal Medicine, Faculty of Medicine, University of Tsukuba, Tsukuba City, Ibaraki, Japan.
Masaru ShimizuDepartment of Internal Medicine, Faculty of Medicine, University of Tsukuba, Tsukuba City, Ibaraki, Japan.
Masahiro YokosawaDepartment of Internal Medicine, Faculty of Medicine, University of Tsukuba, Tsukuba City, Ibaraki, Japan.
Seiji SegawaDepartment of Internal Medicine, Faculty of Medicine, University of Tsukuba, Tsukuba City, Ibaraki, Japan.
Akira IizukaDepartment of Internal Medicine, Faculty of Medicine, University of Tsukuba, Tsukuba City, Ibaraki, Japan.
Reona TanimuraDepartment of Internal Medicine, Faculty of Medicine, University of Tsukuba, Tsukuba City, Ibaraki, Japan.
Hiroto TsuboiDepartment of Internal Medicine, Faculty of Medicine, University of Tsukuba, Tsukuba City, Ibaraki, Japan.
Isao MatsumotoDepartment of Internal Medicine, Faculty of Medicine, University of Tsukuba, Tsukuba City, Ibaraki, Japan.
Takayuki SumidaDepartment of Internal Medicine, Faculty of Medicine, University of Tsukuba, Tsukuba City, Ibaraki, Japan.
University of Tsukuba · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

RORγt+Foxp3+regulatory T (Treg) cells, known as T regulatory 17 cells (Tr17 cells), are a novel subset of Treg cells, which have the potential to regulate the development of experimental autoimmune encephalomyelitis (EAE) thorough a specific repression of T helper 17 (Th17) cell-mediated inflammation. However, the function of Tr17 cells the development of other autoimmune diseases such as autoimmune arthritis remains unclear. Collagen-induced arthritis (CIA) was found to be prolonged in Foxp3creRORγtfl/fl mice, in which Tr17 cells were deleted, compared with Foxp3wtRORγtfl/fl mice. Tr17 cells were significantly increased in ankle joints (AJ) compared with draining lymph nodes after the onset of arthritis. CC chemokine receptor 6 (CCR6) was up-regulated on Tr17 cells compared to RORγt negative Treg cells. CD25, cytotoxic T-lymphocyte antigen 4 (CTLA-4), glucocorticoid-induced TNF-receptor (GITR), and inducible T-cell co-stimulator (ICOS) expression was also up-regulated on Tr17 cells compared to RORγt negative Treg cells. IL-10-producing cells and Blimp-1+ and T-bet+ cells were increased in Tr17 cells compared to RORγt-negative Treg cells. Tr17-enriched Treg cells significantly suppressed proliferation of conventional T cells through IL-10 compared with CCR6-Treg cells. Tr17 cells increased during the clinical course of CIA and accumulated in inflamed joints. Taken together, it appears that Tr17 cells play a crucial role in the regulation of autoimmune arthritis.

Indexed as

Arthritis, ExperimentalEncephalomyelitis, Autoimmune, ExperimentalAnimalsForkhead Transcription FactorsMiceMice, Inbred C57BLNuclear Receptor Subfamily 1, Group F, Member 3Th17 CellsT-Lymphocytes, RegulatoryForkhead Transcription FactorsFoxp3 protein, mouseNuclear Receptor Subfamily 1, Group F, Member 3autoimmune arthritisCD4+ T cellsFoxp3regulatory T cellsRORγtT regulatory 17 cells Tr17 cells

Identifiers

PMID35020849
PMCPMC8982961
OpenAlexW4226137262

What OpenQuestion holds

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Registered trials

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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.