Evidence map›Paper›PMID 23378429›Full record

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

B1a cells enhance susceptibility to infection with virulent Francisella tularensis via modulation of NK/NKT cell responses.

Deborah D Crane, Amanda J Griffin, Tara D Wehrly, Catharine M Bosio

Open access · bronzeAbstract 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 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

26 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Article
  3. The immune response toFrontiers in microbiology · 2025
    Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Effects of BTK signalling in pathogenic microorganism infections.Journal of cellular and molecular medicine · 2019
    Review
  9. B-1 cell responses to infections.Current opinion in immunology · 2019
    Review
  10. Article
  11. Adaptive Immunity toFrontiers in cellular and infection microbiology · 2018
    Review
  12. Article
  13. IL-10 Plays Opposing Roles duringJournal of immunology (Baltimore, Md. : 1950) · 2017
    Article
  14. Article
  15. Article
  16. Article
  17. The role of B-1 cells in inflammation.Immunologic research · 2015
    Review
  18. Article
  19. Article
  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

4 authors at 2 institutions in 1 country.

Deborah D CraneImmunity to Pulmonary Pathogens Section, Laboratory of Intracellular Parasites, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases/National Institutes of Health, Hamilton, MT 59840, USA.
Amanda J Griffin
Tara D Wehrly
Catharine M Bosio
National Institute of Allergy and Infectious Diseases · USNational Institutes of Health · US

Funding

Immunity to Pulmonary InfectionsZIAAI001013 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI BOSIO, CATHARINE · 2009 to 2025
$18.9M
Intramural NIH HHS ZIA AI001013
6 · The paper itself

Abstract

B1a cells are an important source of natural Abs, Abs directed against T-independent Ags, and are a primary source of IL-10. Bruton's tyrosine kinase (btk) is a cytoplasmic kinase that is essential for mediating signals from the BCR and is critical for development of B1a cells. Consequentially, animals lacking btk have few B1a cells, minimal Ab responses, and can preferentially generate Th1-type immune responses following infection. B1a cells have been shown to aid in protection against infection with attenuated Francisella tularensis, but their role in infection mediated by fully virulent F. tularensis is not known. Therefore, we used mice with defective btk (CBA/CaHN-Btk(XID)/J [XID mice]) to determine the contribution of B1a cells in defense against the virulent F. tularensis ssp. tularensis strain SchuS4. Surprisingly, XID mice displayed increased resistance to pulmonary infection with F. tularensis. Specifically, XID mice had enhanced clearance of bacteria from the lung and spleen and significantly greater survival of infection compared with wild-type controls. We revealed that resistance to infection in XID mice was associated with decreased numbers of IL-10-producing B1a cells and concomitant increased numbers of IL-12-producing macrophages and IFN-γ-producing NK/NKT cells. Adoptive transfer of wild-type B1a cells into XID mice reversed the control of bacterial replication. Similarly, depletion of NK/NKT cells also increased bacterial burdens in XID mice. Together, our data suggest B cell-NK/NKT cell cross-talk is a critical pivot controlling survival of infection with virulent F. tularensis.

Indexed as

Genetic Predisposition to DiseaseAnimalsAntibodies, BacterialB-Lymphocyte SubsetsCell CommunicationCells, CulturedExudates and TransudatesFrancisella tularensisKiller Cells, NaturalMiceMice, Inbred CBAMice, Mutant StrainsNatural Killer T-CellsPeritoneumProtein-Tyrosine KinasesSurvival AnalysisAntibodies, BacterialProtein-Tyrosine Kinases

Identifiers

PMID23378429
PMCPMC3594638
OpenAlexW2169702024

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.