Cited by 1,647T-cell and B-cell ImmunologyMultiple Sclerosis Research StudiesPsoriasis: Treatment and Pathogenesis

B cells regulate autoimmunity by provision of IL-10

Fillatreau, Simon, Sweenie, Claire H., McGeachy, Mandy J., Gray, David, Anderton, Stephen M.·2002·Nature Immunology

Abstract

To assess the importance of B cell control of T cell differentiation, we analyzed the course of the T helper type 1 (T(H)1)-driven disease experimental autoimmune encephalomyelitis in mice with an altered B cell compartment. We found that recovery was dependent on the presence of autoantigen-reactive B cells. B cells from recovered mice produced interleukin 10 (IL-10) in response to autoantigen. With a bone marrow chimeric system, we generated mice in which IL-10 deficiency was restricted to B cells but not T cells. In the absence of IL-10 production by B cells, the pro-inflammatory type 1 immune response persisted and mice did not recover. These data show that B cell-derived IL-10 plays a key role in controlling autoimmunity.

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  • Bregs are B cells with regulatory and immunosuppressive functions that maintain immunological homeostasis by producing IL-10, IL-35, and TGFβ, thereby suppressing immunopathology.

    “Bregs is a generic term used to define B cells endowed with regulatory and immunosuppressive functions. They play a crucial role in maintain­ ing immunological homeostasis by producing anti-inflammatory cyto­ kines such as interleukin-10 (IL-10), IL-35, and transforming growth factor-beta (TGFβ ), thereby suppressing immunopathology.”

    From Is there a role for B cells in Alzheimer's disease? (2026) · cites this paper as [54]

  • Mice genetically altered in B cell development, particularly those lacking IL-10-producing B cells, develop uncontrolled autoimmune diseases.

    “Findings demonstrate that mice genetically altered in B cell development, partic­ ularly those lacking IL-10-producing B cells, develop uncontrolled auto­ immune diseases [53,54].”

    From Is there a role for B cells in Alzheimer's disease? (2026) · cites this paper as [54]

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Authors
Fillatreau, S., Sweenie, C. H., McGeachy, M. J., Gray, D., & Anderton, S. M.
Affiliations
University of Edinburgh (GB)
Corresponding author
Anderton, Stephen M.
Venue
Nature Immunology
Published
2002-09-03
Volume
3
Issue
10
Pages
944-950
ISSN
  • 1529-2908 (ISSN-L)
  • 1529-2916
OpenAlex
W2077297620
Cited by
1,647
References
1
Citations by year
2026: 37 · 2025: 45 · 2024: 70 · 2023: 54 · 2022: 70 · 2021: 94 · 2020: 79 · 2019: 84 · 2018: 78 · 2017: 86 · 2016: 99 · 2015: 115 · 2014: 119 · 2013: 91 · 2012: 90
FWCI
8.21
Type
journal article
Language
en
Open access
closed
Locations
  • Nature Immunology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
  • Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
Keywords
B cells, IL-10, autoimmunity, experimental autoimmune encephalomyelitis, T cell differentiation, bone marrow chimerism, recovery from illness, pro-inflammatory response
MeSH terms
Animals, B-Lymphocytes, Encephalomyelitis, Autoimmune, Experimental, Mice, Inbred C57BL, Autoimmunity, Interleukin-10, Mice, Knockout, Th1 Cells, Mice

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