Evidence map›Paper›PMID 21911371›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2011

B cell-derived IL-10 suppresses inflammatory disease in Lyn-deficient mice.

Patrizia Scapini, Chrystelle Lamagna, Yongmei Hu, Karim Lee, Qizhi Tang, Anthony L DeFranco, Clifford A Lowell

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

47 citing papers in PubMed, 80 citations in OpenAlex.

  1. Article
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  6. Frontiers in immunology · 2025
    Article
  7. Review
  8. The role of B cells in cancer development.Frontiers in oncology · 2022
    Review
  9. Article
  10. Review
  11. Article
  12. Modulation of Splenic B Cell Subsets during ExperimentalPathogens (Basel, Switzerland) · 2021
    Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
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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

7 authors at 2 institutions in 2 countries.

Patrizia ScapiniDepartment of Laboratory Medicine and Microbiology/Immunology, University of California, San Francisco, CA 94143, USA. scapini@univr.it
Chrystelle Lamagna
Yongmei Hu
Karim Lee
Qizhi Tang
Anthony L DeFranco
Clifford A Lowell
University of California, San Francisco · USUniversity of Verona · IT

Funding

The contribution of innate immune cells to autoimmunityP01AI078869 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LOWELL, CLIFFORD A · 2008 to 2012
$8.9M
Mechanisms of Neutrophil ActivationR01AI065495 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LOWELL, CLIFFORD A · 2005 to 2017
$3.7M
Signaling by Cytoplasmic Tyrosine Kinases in LeukocytesR01AI068150 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LOWELL, CLIFFORD A · 2006 to 2016
$3.4M
NIAID NIH HHS AI078869NIAID NIH HHS AI65495NIAID NIH HHS AI68150NIAID NIH HHS P01 AI078869NIAID NIH HHS R01 AI065495NIAID NIH HHS R01 AI068150
6 · The paper itself

Abstract

Lyn kinase deficient mice represent a well established genetic model of autoimmune/autoinflammatory disease that resembles systemic lupus erythematosus. We report that IL-10 plays a crucial immunosuppressive role in this model, modulating the inflammatory component of the disease caused by myeloid and T-cell activation. Double-mutant lyn(-/-)IL-10(-/-) mice manifested severe splenomegaly and lymphadenopathy, dramatically increased proinflammatory cytokine production, and severe tissue inflammation. Single-mutant lyn(-/-)mice showed expansion of IL-10-producing B cells. Interestingly, WT B cells adoptively transferred into lyn(-/-) mice showed increased differentiation into IL-10-producing B cells that assumed a similar phenotype to endogenous lyn(-/-) IL-10-producing B cells, suggesting that the inflammatory environment present in lyn(-/-) mice induces IL-10-producing B-cell differentiation. B cells, but not T or myeloid cells, were the critical source of IL-10 able to reduce inflammation and autoimmunity in double mutant lyn(-/-)IL-10(-/-) mice. IL-10 secretion by B cells was also crucial to sustain transcription factor Forkhead Box P3 (Foxp3) expression in regulatory T cells during disease development. These data reveal a dominant immunosuppressive function of B-cell-derived IL-10 in the Lyn-deficient model of autoimmunity, extending our current understanding of the role of IL-10 and IL-10-producing B cells in systemic lupus erythematosus.

Indexed as

AnimalsB-Lymphocytes, RegulatoryCell DifferentiationCytokinesDisease Models, AnimalHumansInflammationInflammation MediatorsInterleukin-10Lupus Erythematosus, SystemicLymphatic DiseasesLymphocyte ActivationMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicCytokinesIL10 protein, mouseInflammation MediatorsInterleukin-10lyn protein-tyrosine kinasesrc-Family Kinases

Identifiers

PMID21911371
PMCPMC3193193
OpenAlexW2118323853

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.