Evidence map›Paper›PMID 18034429›Full record

ArticleEuropean journal of immunology2007

Anti-chromatin antibodies drive in vivo antigen-specific activation and somatic hypermutation of rheumatoid factor B cells at extrafollicular sites.

Robin A Herlands, Jacqueline William, Uri Hershberg, Mark J Shlomchik

Open access · bronzeAbstract read
In one paragraph

Article in European journal of immunology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
2.2field-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

50 citing papers in PubMed, 70 citations in OpenAlex.

  1. Article
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  6. Glucose Requirement of Antigen-Specific Autoreactive B Cells and CD4+ T Cells.Journal of immunology (Baltimore, Md. : 1950) · 2023
    Article
  7. Review
  8. Review
  9. Article
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  12. Targeting B Cells and Plasma Cells in Glomerular Diseases: Translational Perspectives.Journal of the American Society of Nephrology : JASN · 2018
    Review
  13. B Cell-ExtrinsicJournal of immunology (Baltimore, Md. : 1950) · 2017
    Article
  14. Article
  15. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Robin A HerlandsSection of Immunobiology, Yale University School of Medicine, New Haven, CT 06520-8035, USA.
Jacqueline William
Uri Hershberg
Mark J Shlomchik
Yale University · 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
TOLERANCE AND AUTOIMMUNITY IN RF TRANSGENIC MICEP01AI036529 · NIAID · YALE UNIVERSITY · PI FLAVELL, RICHARD A · 1994 to 2006
$9.4M
Activation and regulation of autoreactive B cells in health and diseaseR01AI073722 · NIAID · YALE UNIVERSITY · PI SHLOMCHIK, MARK J · 2008 to 2012
$2.6M
Testing in Vivo Roles of TLRs in Systemic AutoimmunityR01AI061090 · NIAID · YALE UNIVERSITY · PI SHLOMCHIK, MARK J · 2004 to 2004
$168k
NIAID NIH HHS P01 AI036529NIAID NIH HHS P01-AI36529NIAID NIH HHS R01 AI061090NIAID NIH HHS R01 AI073722NIAMS NIH HHS P01 AR050256NIAMS NIH HHS P01-AR050256
6 · The paper itself

Abstract

A dominant type of spontaneous autoreactive B cell activation in murine lupus is the extrafollicular generation of plasmablasts. The factors governing such activation have been difficult to identify due to the stochastic onset and chronic nature of the response. Thus, the ability to induce a similar autoreactive B cell response with a known autoantigen in vivo would be a powerful tool in deciphering how autoimmune responses are initiated. We report here the establishment and characterization of a system to initiate autoreactive extrafollicular B cell responses, using IgG anti-chromatin antibodies, that closely mirrors the spontaneous response. We demonstrate that exogenously administered anti-chromatin antibody, presumably by forming immune complexes with released nuclear material, drives activation of rheumatoid factor B cells in AM14 Tg mice. Anti-chromatin elicits autoreactive B cell activation and development into antibody-forming cells at the T zone/red pulp border. Plasmablast generation occurs equally in BALB/c, MRL/+ and MRL/lpr mice, indicating that an autoimmune-prone genetic background is not required for the induced response. Importantly, infused IgG anti-chromatin induces somatic hypermutation in the absence of a GC response, thus proving the extrafollicular somatic hypermutation pathway. This system provides a window on the initiation of an autoantibody response and reveals authentic initiators of it.

Indexed as

AnimalsAntibodies, AntinuclearAutoimmunityB-Lymphocyte SubsetsChromatinDisease Models, AnimalGenetic Predisposition to DiseaseImmunoglobulin GLupus Erythematosus, SystemicLymphocyte ActivationLymphocyte CooperationMiceMice, Inbred BALB CMice, Inbred MRL lprMice, TransgenicNucleosomesAntibodies, AntinuclearChromatinImmunoglobulin GNucleosomesRheumatoid FactorToll-Like Receptors

Identifiers

PMID18034429
PMCPMC3516908
OpenAlexW2007929292

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.