UCL  IRIS
Institutional Research Information Service
UCL Logo
Please report any queries concerning the funding data grouped in the sections named "Externally Awarded" or "Internally Disbursed" (shown on the profile page) to your Research Finance Administrator. Your can find your Research Finance Administrator at https://www.ucl.ac.uk/finance/research/rs-contacts.php by entering your department
Please report any queries concerning the student data shown on the profile page to:

Email: portico-services@ucl.ac.uk

Help Desk: http://www.ucl.ac.uk/ras/portico/helpdesk
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:
    09/2014
  • Pagination:
    2692, 2702
  • Journal:
    Eur J Immunol
  • Volume:
    44
  • Issue:
    9
  • Status:
    Published
  • Country:
    Germany
  • Language:
    eng
  • 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
Abstract
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.
Publication data is maintained in RPS. Visit https://rps.ucl.ac.uk
 More search options
UCL Researchers
Author
Div of Infection & Immunity
Author
Div of Infection & Immunity
Author
Infection, Immunity & Inflammation Dept
University College London - Gower Street - London - WC1E 6BT Tel:+44 (0)20 7679 2000

© UCL 1999–2011

Search by