Evidence map›Paper›PMID 21776333›Full record

ArticleSelf/nonself2011

A role of IL-1R1 signaling in the differentiation of Th17 cells and the development of autoimmune diseases.

Yonggang Sha, Silva Markovic-Plese

Open access · hybridAbstract read
In one paragraph

Article in Self/nonself, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

22 citing papers in PubMed, 47 citations in OpenAlex.

  1. Trial
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  8. Review
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  11. Increased ratio of Th17 cells to SIGIRRBiomedical reports · 2018
    Article
  12. NLRP3 Inflammasome and IL-33: Novel Players in Sterile Liver Inflammation.International journal of molecular sciences · 2018
    Review
  13. Article
  14. Toll-Like Receptor Pathways in Autoimmune Diseases.Clinical reviews in allergy & immunology · 2016
    Review
  15. Article
  16. Role of IL-17 in Glioma Progression.Journal of spine & neurosurgery · 2013
    Article
  17. Article
  18. Article
  19. IL-1 and T Helper Immune Responses.Frontiers in immunology · 2013
    Article
  20. Article
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

2 authors at 1 institution in 2 countries.

Yonggang ShaDepartment of Neurology; University of North Carolina at Chapel Hill; Chapel Hill, NC USA.
Silva Markovic-Plese
University of North Carolina at Chapel Hill · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

IL-1 cytokine family plays a key role in the innate immune response against pathogen- and danger-associated molecular patterns. More recently, IL-1 receptor type 1 (IL-R1) signaling has been identified as a critical step in the differentiation and commitment of Th17 cells, which mediate the development of autoimmune diseases. Given its significance in the induction of the adoptive immune response, this complex signaling pathway is tightly regulated. Upon binding of IL-1 to IL-1R1, IL-1R accessory protein (AcP) is recruited to form a high affinity IL-1R1-IL-1RAcP heterodimeric receptor, which initiates the downstream signaling cascade. Multiple negative regulators of this pathway, including inhibitory membrane-bound IL-RII, secreted soluble (s)IL-1RI, sIL-RII and sIL-1RAcP, the regulatory IL-1R1 antagonist (IL-1R1a) and the IL-1R1-signlaing-induced single Ig-IL-1R-related (SIGIRR), provide a negative feedback control of this pathway, and suppress excessive IL-1 signaling and Th17 cell differentiation. IL-1R1 signaling induces human Th17 cell differentiation, leading to the expression of IL-1R-associated protein kinase (IRAK)4 and retinoic acid-related orphan nuclear hormone receptor (ROR), Th17 cell lineage transcription factors, which together with signal transducer and activator of the transcription (STAT)3, activate this cell lineage's specific cytokine expression profile, including IL-17A, IL-17F, IL-21 and IL-22. Given the role of IL-1 signaling and Th17 cells in the development of the autoinflammatory and autoimmune diseases, therapeutic strategies inhibiting IL-1R1 signaling are discussed as a novel approach for the treatment of autoimmune diseases and particularly multiple sclerosis (MS).

Identifiers

PMID21776333
PMCPMC3136902
OpenAlexW2019189163

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.