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B Cell Depletion Reduces the Number of Autoreactive T Helper Cells and Prevents Glucose-6-Phosphate Isomerase-Induced Arthritis

Authors
Journal
PLoS ONE
1932-6203
Publisher
Public Library of Science
Publication Date
Volume
6
Issue
9
Identifiers
DOI: 10.1371/journal.pone.0024718
Keywords
  • Research Article
  • Biology
  • Immunology
  • Immune Cells
  • B Cells
  • T Cells
  • Immune System
  • Cytokines
  • Immunity
  • Immunoregulation
  • Autoimmunity
  • Immunoglobulins
  • Medicine
  • Clinical Immunology
  • Autoimmune Diseases
  • Rheumatoid Arthritis
  • Antigen-Presenting Cells
  • Immune Tolerance
  • Inflammation
  • Immunologic Techniques
  • Immunoassays
  • Immune Response
  • Immunopathology
Disciplines
  • Biology
  • Medicine

Abstract

The therapeutic benefit of B cell depletion in patients with rheumatoid arthritis has provided proof of concept that B cells are relevant for the pathogenesis of arthritis. It remains unknown which B cell effector functions contribute to the induction or chronification of arthritis. We studied the clinical and immunological effects of B cell depletion in glucose-6-phosphate isomerase-induced arthritis. We targeted CD22 to deplete B cells. Mice were depleted of B cells before or after immunization with glucose-6-phosphate isomerase (G6PI). The clinical and histological effects were studied. G6PI-specific antibody responses were measured by ELISA. G6PI-specific T helper (Th) cell responses were assayed by polychromatic flow cytometry. B cell depletion prior to G6PI-immunization prevented arthritis. B cell depletion after immunization ameliorated arthritis, whereas B cell depletion in arthritic mice was ineffective. Transfer of antibodies from arthritic mice into B cell depleted recipients did not reconstitute arthritis. B cell depleted mice harbored much fewer G6PI-specific Th cells than control animals. B cell depletion prevents but does not cure G6PI-induced arthritis. Arthritis prevention upon B cell depletion is associated with a drastic reduction in the number of G6PI-specific effector Th cells.

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