Evidence map›Paper›PMID 21306913›Full record

ReviewSeminars in immunology2011

Toll-like receptor driven B cell activation in the induction of systemic autoimmunity.

Nathaniel M Green, Ann Marshak-Rothstein

Open access · greenAbstract readReview
In one paragraph

Review in Seminars in immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers.

0numbers the graph read from it
0cells of the map it votes in
113citing papers in PubMed
9.9field-weighted citation impact, top 1% 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

113 citing papers in PubMed, 199 citations in OpenAlex.

  1. Trial
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  10. Role of Sam68 as an adaptor protein in inflammatory signaling.Cellular and molecular life sciences : CMLS · 2024
    Review
  11. Review
  12. Article
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  15. Review
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  18. The solute carrier SLC15A4 is required for optimal trafficking of nucleic acid-sensing TLRs and ligands to endolysosomes.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  19. Gene regulation in time and space during X-chromosome inactivation.Nature reviews. Molecular cell biology · 2022
    Review
  20. Review

53 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Nathaniel M GreenDepartment of Microbiology, Boston University School of Medicine, Boston, MA 02118, USA. nmgreen@bu.edu
Ann Marshak-Rothstein
Boston University · USUniversity of Massachusetts Chan Medical School · US

Funding

Toll-Like Receptors in Systemic Autoimmune DiseaseP01AR050256 · NIAMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI SHLOMCHIK, MARK J · 2004 to 2013
$13.4M
B CELL HYPERACTIVITY IN AUTOIMMUNITYR01AR035230 · NIAMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI MARSHAK-ROTHSTEIN, ANN · 1986 to 2010
$3.2M
NIAMS NIH HHS P01 AR050256NIAMS NIH HHS R01 AR035230
6 · The paper itself

Abstract

Studies over the past decade have demonstrated a key role for pattern recognition receptors in the activation of autoreactive B cells. Self reactive B cells that manage to escape negative selection often express relatively low affinity receptors for self antigens (ignorant B cells), and can only be activated by integrating a relatively weak BCR signal with signals from additional receptors. Members of the toll-like receptor (TLR) gene family, and especially the nucleic acid binding receptors TLR 7, 8 and 9, appear to play a key role in this regard and promote the production of autoantibodies reactive with DNA- or RNA-associated autoantigens. These autoantibodies are able to form immune complexes with soluble or cell-bound ligands, and these immune complexes can in turn activate a second round of proinflammatory cells that further contribute to the autoimmune disease process. Recent data have emerged showing a pathogenic role for TLR7, with an opposing, protective role for TLR9. Targeting these disregulated pathways offers a therapeutic opportunity to treat autoimmune diseases without crippling the entire immune system. Further understanding of the role of specific receptors, cell subsets, and inhibitory signals that govern these TLR-associated pathways will enable future therapeutics to be tailored to specific categories of autoimmune disease.

Indexed as

AutoimmunityLymphocyte ActivationAnimalsAutoantibodiesB-LymphocytesHumansInterferon Type IToll-Like ReceptorsAutoantibodiesInterferon Type IToll-Like Receptors

Identifiers

PMID21306913
PMCPMC3070769
OpenAlexW2055754872

What OpenQuestion holds

Textmetadata
LicenceTDM
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.