Evidence map›Paper›PMID 26496462›Full record

ArticleClinical and experimental immunology2016

Pathogenic T helper type 17 cells contribute to type 1 diabetes independently of interleukin-22.

S M Bellemore, E Nikoopour, O Krougly, E Lee-Chan, L A Fouser, B Singh

Open access · bronzeAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

21 citing papers in PubMed, 33 citations in OpenAlex.

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  9. Adenoviral gene transfer of a single-chain IL-23 induces psoriatic arthritis-like symptoms in NOD mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  10. IL-17 and limits of success.Cellular immunology · 2019
    Review
  11. Article
  12. Article
  13. [Protective effect of vitamin A on residual pancreatic β cell function in children with type 1 diabetes mellitus].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2018
    Article
  14. Review
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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

6 authors at 2 institutions in 2 countries.

S M BellemoreCentre for Human Immunology and Department of Microbiology and Immunology and Robarts Research Institute, University of Western Ontario, London, Ontario, Canada.
E NikoopourCentre for Human Immunology and Department of Microbiology and Immunology and Robarts Research Institute, University of Western Ontario, London, Ontario, Canada.
O KrouglyCentre for Human Immunology and Department of Microbiology and Immunology and Robarts Research Institute, University of Western Ontario, London, Ontario, Canada.
E Lee-ChanCentre for Human Immunology and Department of Microbiology and Immunology and Robarts Research Institute, University of Western Ontario, London, Ontario, Canada.
L A FouserInflammation and Immunology, Biotherapeutics Research and Development, Pfizer Inc., Cambridge, MA, 02140, USA.
B SinghCentre for Human Immunology and Department of Microbiology and Immunology and Robarts Research Institute, University of Western Ontario, London, Ontario, Canada.
Western University · CAPfizer (United States) · US

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

We have shown that pathogenic T helper type 17 (Th17) cells differentiated from naive CD4(+) T cells of BDC2·5 T cell receptor transgenic non-obese diabetic (NOD) mice by interleukin (IL)-23 plus IL-6 produce IL-17, IL-22 and induce type 1 diabetes (T1D). Neutralizing interferon (IFN)-γ during the polarization process leads to a significant increase in IL-22 production by these Th17 cells. We also isolated IL-22-producing Th17 cells from the pancreas of wild-type diabetic NOD mice. IL-27 also blocked IL-22 production from diabetogenic Th17 cells. To determine the functional role of IL-22 produced by pathogenic Th17 cells in T1D we neutralized IL-22 in vivo by using anti-IL-22 monoclonal antibody. We found that blocking IL-22 did not alter significantly adoptive transfer of disease by pathogenic Th17 cells. Therefore, IL-22 is not required for T1D pathogenesis. The IL-22Rα receptor for IL-22 however, increased in the pancreas of NOD mice during disease progression and based upon our and other studies we suggest that IL-22 may have a regenerative and protective role in the pancreatic islets.

Indexed as

Adoptive TransferAnimalsAntibodies, BlockingAntibodies, NeutralizingAutoimmunityCell DifferentiationDiabetes Mellitus, Type 1Disease Models, AnimalDisease ProgressionInterferon-gammaInterleukin-22Interleukin-27InterleukinsIslets of LangerhansMice, Inbred NODPancreasAntibodies, BlockingAntibodies, NeutralizingInterferon-gammaInterleukin-22interleukin-22 receptorInterleukin-27InterleukinsReceptors, InterleukinautoimmunityIL-22Th17 cellstype 1 diabetes

Identifiers

PMID26496462
PMCPMC4750601
OpenAlexW2285127602

What OpenQuestion holds

Textmetadata
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.