Evidence map›Paper›PMID 17556590›Full record

ArticleThe American journal of pathology2007

CD19 expression in B cells is important for suppression of contact hypersensitivity.

Rei Watanabe, Manabu Fujimoto, Nobuko Ishiura, Yoshihiro Kuwano, Hiroko Nakashima, Norihito Yazawa, Hitoshi Okochi, Shinichi Sato, Thomas F Tedder, Kunihiko Tamaki

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 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
3.9field-weighted citation impact, top 7% 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, 116 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. NFATc1 Abrogation in B Cells Ameliorates Contact Hypersensitivity Responses.International journal of molecular sciences · 2025
    Article
  5. Breg-Mediated Immunoregulation in the Skin.International journal of molecular sciences · 2024
    Review
  6. Review
  7. Article
  8. TLR9 Signaling Is Required for theInternational journal of molecular sciences · 2023
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. HMGB1-mediated chromatin remodeling attenuatesProceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  14. Review
  15. Article
  16. Regulatory and IgEMethods in molecular biology (Clifton, N.J.) · 2021
    Article
  17. Article
  18. Resident Memory B Cells.Viral immunology · 2020
    Review
  19. Article
  20. Review
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

10 authors at 6 institutions in 2 countries.

Rei WatanabeDepartment of Dermatology, Faculty of Medicine, University of Tokyo, Tokyo, Japan.
Manabu Fujimoto
Nobuko Ishiura
Yoshihiro Kuwano
Hiroko Nakashima
Norihito Yazawa
Hitoshi Okochi
Shinichi Sato
Thomas F Tedder
Kunihiko Tamaki
The University of Tokyo · JPTokyo University of Science · JPDuke Medical Center · USKanazawa University · JPNagasaki University · JPSaitama International Medical Center · JP

Funding

Supplement - Inflammatory Triggers in B Cell AutoimmunityU19AI056363 · NIAID · DUKE UNIVERSITY · PI ST. CLAIR, EUGENE WILLIAM · 2003 to 2017
$35.3M
CD22 Regulation of B Lymphocyte Function and SurvivalR01CA096547 · NCI · DUKE UNIVERSITY · PI TEDDER, THOMAS F · 2003 to 2007
$1.3M
MS4A Family Members in Health and DiseaseR01CA105001 · NCI · DUKE UNIVERSITY · PI TEDDER, THOMAS F · 2004 to 2008
$1.2M
NCI NIH HHS CA105001NCI NIH HHS CA96547NCI NIH HHS R01 CA096547NCI NIH HHS R01 CA105001NIAID NIH HHS AI56363NIAID NIH HHS U19 AI056363
6 · The paper itself

Abstract

Contact hypersensitivity (CHS) is a cutaneous immune reaction mediated mainly by antigen-specific effector T cells and is regarded as a model for Th1/Tc1-mediated inflammation. However, recent reports have suggested pivotal roles of B cells in CHS. CD19 serves as a positive B-cell response regulator that defines signaling thresholds critical for B-cell responses. In the current study, we assessed the role of the B-cell-specific surface molecule CD19 on the development of CHS by examining CD19-deficient mice. Although CD19-deficient mice are hyposensitive to a variety of transmembrane signals, CD19 loss resulted in increased and prolonged reaction of CHS, suggesting an inhibitory role of CD19 expression in CHS. Sensitized lymph nodes and elicited ear lesions from CD19-deficient mice exhibited Th1/Tc1-shifted cytokine profile with increased interferon-gamma expression and decreased interleukin-10 expression. Adoptive transfer experiments revealed that CD19 expression in recipient mice was required for optimal suppression of CHS response, indicating its role in the elicitation phase. Furthermore, spleen B cells, especially marginal zone B cells, from wild-type mice were able to normalize exaggerated CHS reactions in CD19-deficient mice. Thus, CD19 expression in B cells is critical for termination of CHS responses, possibly through the function of regulatory B cells.

Indexed as

Adoptive TransferAnimalsAntigens, CD19B-LymphocytesCD4-Positive T-LymphocytesCell ProliferationDendritic CellsDermatitis, ContactEarFlow CytometryGenotypeInflammationInterferon-gammaInterleukin-10Interleukin-2Interleukin-4Antigens, CD19Interferon-gammaInterleukin-10Interleukin-2Interleukin-4

Identifiers

PMID17556590
PMCPMC1934538
OpenAlexW2017602089

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.