Evidence map›Paper›PMID 23619359›Full record

ArticleThe Journal of clinical investigation2013

Autoimmunity risk alleles: hotspots in B cell regulatory signaling pathways.

John C Cambier

Open access · bronzeAbstract readComment
In one paragraph

Article in The Journal of clinical investigation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 8% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Pooled it
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  20. PTPN22: the archetypal non-HLA autoimmunity gene.Nature reviews. Rheumatology · 2014
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

John C CambierIntegrated Department of Immunology, University of Colorado School of Medicine and National Jewish Health, Denver, Colorado, USA. cambierj@njhealth.org
National Jewish Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autoimmunity is the consequence of the combination of genetic predisposition and environmental effects, such as infection, injury, and constitution of the gut microbiome. In this edition of the JCI, Dai et al. describe the use of knockin technology to test the mechanism of action of a polymorphism in the protein tyrosine phosphatase nonreceptor 22 (PTPN22) (LYP) that is associated with susceptibility to multiple autoimmune diseases. The function of this allele, and that of a disproportionate number of autoimmune disease risk alleles, suggests that inhibitory signaling pathways that maintain B lymphocyte immune tolerance may represent an Achilles' heel in the prevention of autoimmunity.

Indexed as

AnimalsAutoimmunityMaleProtein Tyrosine Phosphatase, Non-Receptor Type 22Protein Tyrosine Phosphatase, Non-Receptor Type 22Ptpn22 protein, mouse

Identifiers

PMID23619359
PMCPMC3635745
OpenAlexW2015867761

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.