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Publication Detail
Exacerbated experimental arthritis in Wiskott-Aldrich syndrome protein deficiency: modulatory role of regulatory B cells.
  • Publication Type:
    Journal article
  • Publication Sub Type:
    Clinical Trial
  • Authors:
    Bouma G, Carter NA, Recher M, Malinova D, Adriani M, Notarangelo LD, Burns SO, Mauri C, Thrasher AJ
  • Publication date:
  • Pagination:
    2692, 2702
  • Journal:
    Eur J Immunol
  • Volume:
  • Issue:
  • Status:
  • Country:
  • Language:
  • Keywords:
    Arthritis, Immune regulation, Regulatory B cells, Regulatory T cell, Th17 cells, Wiskott-Aldrich syndrome protein, Animals, Arthritis, Experimental, Autoimmune Diseases, B-Lymphocyte Subsets, Female, Humans, Interleukin-10, Male, Mice, Mice, Knockout, T-Lymphocytes, Regulatory, Th17 Cells, Wiskott-Aldrich Syndrome Protein
Patients deficient in the cytoskeletal regulator Wiskott-Aldrich syndrome protein (WASp) are predisposed to varied autoimmunity, suggesting it has an important controlling role in participating cells. IL-10-producing regulatory B (Breg) cells are emerging as important mediators of immunosuppressive activity. In experimental, antigen-induced arthritis WASp-deficient (WASp knockout [WAS KO]) mice developed exacerbated disease associated with decreased Breg cells and regulatory T (Treg) cells, but increased Th17 cells in knee-draining LNs. Arthritic WAS KO mice showed increased serum levels of B-cell-activating factor, while their B cells were unresponsive in terms of B-cell-activating factor induced survival and IL-10 production. Adoptive transfer of WT Breg cells ameliorated arthritis in WAS KO recipients and restored a normal balance of Treg and Th17 cells. Mice with B-cell-restricted WASp deficiency, however, did not develop exacerbated arthritis, despite exhibiting reduced Breg- and Treg-cell numbers during active disease, and Th17 cells were not increased over equivalent WT levels. These findings support a contributory role for defective Breg cells in the development of WAS-related autoimmunity, but demonstrate that functional competence in other regulatory populations can be compensatory. A properly regulated cytoskeleton is therefore important for normal Breg-cell activity and complementation of defects in this lineage is likely to have important therapeutic benefits.
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