CD40 mediates downregulation of CD32B on specific memory B cell populations in rheumatoid arthritis

Xiaoyu Zhang, Erin Burch, Ling Cai, Edward So, Fleesie Hubbard, Eric L. Matteson, Scott E. Strome

Research output: Contribution to journalArticle

13 Scopus citations

Abstract

Altered B cell function is important in the pathogenesis of rheumatoid arthritis (RA). In this report, we show that patients with active RA have an increased frequency of CD32B low/neg cells in the CD27+IgD - memory B cell subset and that these changes are associated with phenotypic and functional B cell activation. Studies using PBMCs from healthy donors revealed that downregulation of CD32B on B cells is mediated by CD40-CD40L interactions and is potentiated by IL-4 and inhibited by both IL-10 and IL-21. These findings appear physiologically relevant because CD4 T cell expression of CD40L correlated with the frequency of CD32B low/neg cells in the CD27+IgD- memory B subset in patients with RA. Our data support a model in which high levels of CD40L, present on circulating T cells in patients with RA, causes B cell activation and CD32B downregulation, resulting in secondary protection of memory B cells from CD32B-mediated cell death.

Original languageEnglish (US)
Pages (from-to)6015-6022
Number of pages8
JournalJournal of Immunology
Volume190
Issue number12
DOIs
StatePublished - Jun 15 2013

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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