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BAFF-driven autoimmunity requires CD19 expression.

Kirsten A Fairfax1, Evelyn Tsantikos2, William A Figgett2

  • 1Faculty of Medicine, Nursing and Health Sciences, Department of Immunology, Central Clinical School, Monash University, Commercial Rd, Melbourne 3004, Australia; The Walter and Eliza Hall Institute of Medical Research, Molecular Medicine Division, 1G Royal Parade, Melbourne 3052, Australia; The Department of Experimental Medicine, University of Melbourne, Parkville, Victoria 3052, Australia.

Journal of Autoimmunity
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PubMed
Summary

Excessive B cell activating factor (BAFF) causes autoimmunity. This study found that B1b B cells, not other innate-like B cells, are essential for developing autoimmune disease in BAFF-transgenic mice.

Keywords:
AutoimmunityB1b cellsBAFFBAFF-transgenicCD19MZ B cells

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Area of Science:

  • Immunology
  • Autoimmunity
  • B cell biology

Background:

  • B cell activating factor (BAFF) is crucial for B cell survival and maturation.
  • BAFF-transgenic (BAFF-Tg) mice exhibit T cell-independent, MyD88-dependent autoimmunity resembling systemic lupus erythematosus (SLE).
  • Toll-like receptor (TLR) signaling implicates innate B cells, specifically marginal zone (MZ) and B1 B cells, in autoantibody production.

Purpose of the Study:

  • To investigate the specific pathogenic B cell subset responsible for BAFF-induced autoimmunity.
  • To test the hypothesis that B1b B cells are the critical drivers of autoimmune disease in BAFF-Tg mice.

Main Methods:

  • Generated BAFF-Tg mice deficient in B1a, B1b, and MZ B cells by crossing with CD19-deficient mice (BTg-CD19(-/-)).
  • Assessed autoantibody production, splenomegaly, kidney pathology, and overall autoimmune signs in the generated mouse model.

Main Results:

  • BTg-CD19(-/-) mice were protected from autoantibodies, splenomegaly, and kidney pathology.
  • These mice showed no signs of autoimmunity, indicating the absence of pathogenic B cells.
  • Loss of B1a, B1b, and MZ B cells completely prevented disease development.

Conclusions:

  • B1b B cells are sufficient and potentially required for the development of autoimmunity in BAFF-Tg mice.
  • Excessive BAFF-induced autoimmunity necessitates both B1b B cells and CD19 signaling.
  • Targeting B1b B cells could be a therapeutic strategy for BAFF-mediated autoimmune diseases.