Evidence map›Paper›PMID 28239656›Full record

ArticleJCI insight2017

Autoreactive helper T cells alleviate the need for intrinsic TLR signaling in autoreactive B cell activation.

Josephine R Giles, Adriana Turqueti Neves, Ann Marshak-Rothstein, Mark J Shlomchik

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2017. 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
0.4field-weighted citation impact, top 40% 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, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Glucose Requirement of Antigen-Specific Autoreactive B Cells and CD4+ T Cells.Journal of immunology (Baltimore, Md. : 1950) · 2023
    Article
  5. T cell help in the autoreactive germinal center.Scandinavian journal of immunology · 2022
    Review
  6. Review
  7. Review
  8. Article
  9. Generation of T Cell Receptor Retrogenic Mice.Current protocols in immunology · 2019
    Article
  10. Review
  11. 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

4 authors at 3 institutions in 1 country.

Josephine R GilesDepartments of Laboratory Medicine and Immunobiology, Yale University School of Medicine, New Haven, Connecticut, USA.
Adriana Turqueti NevesDepartment of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.
Ann Marshak-RothsteinDivision of Rheumatology, Department of Medicine, University of Massachusetts School of Medicine, Worcester, Massachusetts, USA.
Mark J ShlomchikDepartments of Laboratory Medicine and Immunobiology, Yale University School of Medicine, New Haven, Connecticut, USA.
Yale University · USUniversity of Massachusetts Chan Medical School · USUniversity of Pittsburgh · 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
THE ROLE OF B CELLS IN LUPUS NEPHRITIS AND VASCULITISR01AR044077 · NIAMS · YALE UNIVERSITY · PI SHLOMCHIK, MARK J · 1997 to 2016
$6.2M
Investigating How TLR7 Activates and TLR9 Regulates Systemic AutoimmunityR37AI118841 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SHLOMCHIK, MARK J · 2016 to 2025
$4.2M
Distinct Functional Outcomes of BCR/TLR7 and BCR/TLR9 Co-engagementR01AR066808 · NIAMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI MARSHAK-ROTHSTEIN, ANN · 2015 to 2019
$2.6M
NIAID NIH HHS R37 AI118841NIAMS NIH HHS P01 AR050256NIAMS NIH HHS R01 AR044077NIAMS NIH HHS R01 AR066808
6 · The paper itself

Abstract

T cells play a significant role in the pathogenesis of systemic autoimmune diseases, including systemic lupus erythematosus; however, there is relatively little information on the nature and specificity of autoreactive T cells. Identifying such cells has been technically difficult because they are likely to be rare and low affinity. Here, we report a method for identifying autoreactive T cell clones that recognize proteins contained in autoantibody immune complexes, providing direct evidence that functional autoreactive helper T cells exist in the periphery of normal mice. These T cells significantly enhanced autoreactive B cell proliferation and altered B cell differentiation in vivo. Most importantly, these autoreactive T cells were able to rescue many aspects of the TLR-deficient AM14 (anti-IgG2a rheumatoid factor) B cell response, suggesting that TLR requirements can be bypassed. This result has implications for the efficacy of TLR-targeted therapy in the treatment of ongoing disease.

Indexed as

AnimalsAntigen-Antibody ComplexAutoantibodiesAutoimmunityB-LymphocytesDNA-Binding ProteinsLymphocyte ActivationMembrane GlycoproteinsMiceMice, KnockoutReceptors, Antigen, T-Cell, alpha-betaSignal TransductionT-Lymphocytes, Helper-InducerToll-Like Receptor 7Toll-Like Receptor 9Toll-Like ReceptorsAntigen-Antibody ComplexAutoantibodiesDNA-Binding ProteinsMembrane GlycoproteinsRag2 protein, mouseReceptors, Antigen, T-Cell, alpha-betaTlr7 protein, mouseTlr9 protein, mouseToll-Like Receptor 7Toll-Like Receptor 9Toll-Like Receptors

Identifiers

PMID28239656
PMCPMC5313065
OpenAlexW2588396304

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.