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Cited by 699Multiple Sclerosis Research StudiesT-cell and B-cell ImmunologyPsoriasis: Treatment and Pathogenesis

Experimental Autoimmune Encephalomyelitis Induction in Genetically B Cell–deficient Mice

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Wolf, Susan D., Dittel, Bonnie N., Hardardottir, Fridrika, Janeway, Charles A.·1996·The Journal of Experimental Medicine
DOI 10.1084/jem.184.6.2271PMC PMC2196394
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Abstract

Experimental autoimmune encephalomyelitis (EAE) is an animal model for autoimmune central nervous system disease mediated by CD4 T cells. To examine the role of B cells in the induction of EAE, we used B10.PL (I-Au) mice rendered deficient in B cells by deletion of their μ chain transmembrane region (B10.PLμMT). By immunizing B10.PL and B10.PLμMT mice with the NH-terminal myelin basic protein encephalitogenic peptide Ac1-11, we observed no difference in the onset or severity of disease in the absence of mature B cells. There was, however, a greater variation in disease onset, severity, and especially of recovery in the B cell–deficient mice compared to controls. B10.PLμMT mice rarely returned to normal in the absence of B cells. Taken together, our data suggest that B cells do not play a role in the activation of encephalitogenic T cells, but may contribute to the immune modulation of acute EAE. The mechanisms to explain these effects are discussed.

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  • 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 [53]

    The Abstract and Discussion report that genetically B-cell-deficient mice developed induced EAE and recovered less completely than controls. They do not show that the mice developed uncontrolled autoimmune diseases generally. The Results measured IL-10 transcripts in CD4+ T cells, not a specific loss of IL-10-producing B cells. Page numbers were not supplied in our copy. (LLM, conf=0.88)

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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 [53]

    The Discussion proposes that B cells may help regulate immune responses during EAE, which supports the broad regulatory role attributed to them. It does not define Bregs or show that B cells produce IL-10, IL-35, or TGFβ; it identifies T cells as producers of IL-10 and TGF-β1 and does not mention IL-35. (LLM, conf=0.86)

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Authors
Wolf, S. D., Dittel, B. N., Hardardottir, F., & Janeway, C. A.
Affiliations
Howard Hughes Medical Institute (US)
ORCID
Dittel, Bonnie N.
Venue
The Journal of Experimental Medicine
Publisher
Rockefeller University Press
Published
1996-12-01
Volume
184
Issue
6
Pages
2271-2278
ISSN
  • 0022-1007 (ISSN-L)
  • 1540-9538
DOI
10.1084/jem.184.6.2271
PMC
PMC2196394
OpenAlex
W2128733540
Cited by
699
References
0
Citations by year
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FWCI
14.51
Type
journal article
Language
en
Open access
Locations
  • The Journal of Experimental Medicine (publishedVersion)
  • PubMed Central (publishedVersion, cc-by-nc-sa)
  • PubMed (publishedVersion)
Funders
  • W. M. Keck Foundation
  • National Institute of Allergy and Infectious Diseases (AI36529, P01AI036529)
Topics
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
  • Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
Keywords
experimental autoimmune encephalomyelitis, B cell deficiency, CD4+ T cell activation, immunomodulation, recovery from illness, autoimmune central nervous system disease, encephalitogenic T cells
MeSH terms
Amino Acid Sequence, Animals, B-Lymphocytes, Base Sequence, Encephalomyelitis, Autoimmune, Experimental, Flow Cytometry, Immunoglobulin mu-Chains, Lymphocyte Activation, Mice, Inbred C57BL, Mice, Mutant Strains, Molecular Sequence Data, Peptide Fragments, RNA, Messenger, T-Lymphocytes, Transcription, Genetic, Polymerase Chain Reaction, Cytokines, Sequence Deletion, DNA Primers, Mice

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