Evidence map›Paper›PMID 23365079›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2013

Rheumatoid factor B cell memory leads to rapid, switched antibody-forming cell responses.

Rebecca A Sweet, Jaime L Cullen, Mark J Shlomchik

Open access · hybridAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 2 pooled it
2.8field-weighted citation impact, top 9% 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

23 citing papers in PubMed, 2 syntheses or guidelines pooled it, 34 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Dysregulation of T Follicular Helper Cells in Lupus.Journal of immunology (Baltimore, Md. : 1950) · 2019
    Review
  9. Observational
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Risk Factors for Melanoma Among Survivors of Non-Hodgkin Lymphoma.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2015
    Article
  18. Article
  19. Review
  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

3 authors at 1 institution in 1 country.

Rebecca A SweetDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.
Jaime L Cullen
Mark J Shlomchik
Yale University · US

Funding

Murine Memory B Cell Development and FunctionR01AI043603 · NIAID · YALE UNIVERSITY · PI MARK J SHLOMCHIK · 1998 to 2026
$9.7M
Activation and regulation of autoreactive B cells in health and diseaseR01AI073722 · NIAID · YALE UNIVERSITY · PI SHLOMCHIK, MARK J · 2008 to 2012
$2.6M
B Cell Memory Development During Systemic AutoimmunityF31AI071694 · NIAID · YALE UNIVERSITY · PI SWEET, REBECCA A · 2006 to 2008
$127k
NIAID NIH HHS 1F31-AI071694NIAID NIH HHS F31 AI071694NIAID NIH HHS R01 AI043603NIAID NIH HHS R01 AI073722NIAID NIH HHS R01-AI073722
6 · The paper itself

Abstract

B cells are critical in the initiation and maintenance of lupus. Autoreactive B cells clonally expand, isotype switch, and mutate--properties associated with memory B cells (MBCs), which are typically generated via germinal centers. The development and functions of autoreactive MBCs in lupus are poorly understood. Moreover, mounting evidence implicates the extrafollicular (EF) response in the generation of switched and mutated autoantibodies that are driven by BCR and TLR corecognition, raising the question of whether MBCs are generated in this context. In this study, we investigated autoreactive MBC generation associated with this type of response. We transferred B cells from AM14 site-directed BCR transgenic mice into nontransgenic normal recipients and elicited an EF response with anti-chromatin Ab, as in prior studies. By following the fate of the stimulated cells at late time points, we found that AM14 B cells persisted at increased frequency for up to 7 wk. Furthermore, these cells had divided in response to Ag but were subsequently quiescent, with a subset expressing the memory marker CD73. These cells engendered rapid, isotype-switched secondary plasmablast responses upon restimulation. Both memory and rapid secondary responses required T cell help to develop, emphasizing the need for T-B collaboration for long-term self-reactivity. Thus, using this model system, we show that the EF response generated persistent and functional MBCs that share some, but not all, of the characteristics of traditional MBCs. Such cells could play a role in chronic or flaring autoimmune disease.

Indexed as

Autoimmunity5'-NucleotidaseAdoptive TransferAnimalsAntibodiesAutoantibodiesB-LymphocytesCell CommunicationCell ProliferationChromatinFemaleGene ExpressionImmunologic MemoryLymphocyte ActivationMiceMice, Transgenic5'-NucleotidaseAntibodiesAutoantibodiesChromatinReceptors, Antigen, T-CellRheumatoid Factor

Identifiers

PMID23365079
PMCPMC3578004
OpenAlexW2126152995

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.