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Cited by 978T-cell and B-cell ImmunologyInflammatory Bowel DiseasePsoriasis: Treatment and Pathogenesis

Chronic Intestinal Inflammatory Condition Generates IL-10-Producing Regulatory B Cell Subset Characterized by CD1d Upregulation

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Mizoguchi, Atsushi, Mizoguchi, Emiko, Takedatsu, Hidetoshi, Blumberg, Richard S, Bhan, Atul K·2002·Immunity
DOI 10.1016/s1074-7613(02)00274-1
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Abstract

B cells possess a variety of immune functions that are involved in normal and abnormal immune responses, including autoimmune disorders. Through murine models of intestinal inflammation, we here demonstrate a B cell subset that is induced in gut-associated lymphoid tissues and is characterized by CD1d upregulation. This B cell subset appears under a chronic inflammatory environment, produces IL-10, and suppresses progression of intestinal inflammation by downregulating inflammatory cascades associated with IL-1 upregulation and STAT3 activation rather than by altering polarized T helper responses. This study indicates that B cells, by producing cytokines such as IL-10, can act as regulatory cells in immunologically mediated inflammatory reactions.

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  • Bregs numbers and their suppressive abilities are often increased in response to chronic inflammation or autoimmune diseases.

    “Bregs numbers and their suppressive abilities are often increased in response to chronic inflammation or autoimmune diseases [59,61].”

    From Is there a role for B cells in Alzheimer's disease? (2026) · cites this paper as [61]

    The Results (page unavailable) show that gut-associated B cells upregulated CD1d in mice with colitis, and transfer experiments show that these cells suppressed intestinal inflammation. The paper does not establish that Breg numbers and suppressive abilities are often increased across chronic inflammatory or autoimmune diseases; it reports no difference in the number of splenic CD1d-high B cells between diseased and control mice. (LLM, conf=0.85)

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Cited by

Sorted by citations

Authors
Mizoguchi, A., Mizoguchi, E., Takedatsu, H., Blumberg, R. S., & Bhan, A. K.
Affiliations
  • Massachusetts General Hospital (US)
  • Brigham and Women's Hospital (US)
Corresponding author
Mizoguchi, Atsushi
ORCID
Venue
Immunity
Publisher
Elsevier BV
Published
2002-02
Volume
16
Issue
2
Pages
219-230
ISSN
1074-7613 (ISSN-L)
DOI
10.1016/s1074-7613(02)00274-1
OpenAlex
W1970742017
Cited by
978
References
1
Citations by year
2026: 19 · 2025: 32 · 2024: 44 · 2023: 33 · 2022: 34 · 2021: 51 · 2020: 46 · 2019: 55 · 2018: 42 · 2017: 51 · 2016: 46 · 2015: 58 · 2014: 79 · 2013: 49 · 2012: 55
FWCI
6.04
Type
journal article
Language
en
Open access
Licence
Locations
  • Immunity (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Institute of Diabetes and Digestive and Kidney Diseases (DK51362, DK 47677, DK 44319, DK53056, DK 34584, DK 43351, R01DK047677, R01DK051362, P30DK043351)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Inflammatory Bowel Disease
  • Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
Keywords
regulatory B cells, IL-10, CD1d, intestinal inflammation, gut-associated lymphoid tissue, B cell subsets, interleukin-1, STAT3, immunosuppression, autoimmune disease, chronic inflammation
MeSH terms
Animals, Chronic Disease, Colitis, Colon, Female, Lymphoid Tissue, Male, Mice, Inbred C57BL, Up-Regulation, B-Lymphocyte Subsets, Interleukin-10, Mice, Knockout, Disease Progression, Antigens, CD1, Mice, Antigens, CD1d

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