Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 105, Issue 35, Pages 13009-13014Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0806874105
Keywords
autoimmunity; B lymphocytes; tolerance; autoantibody
Categories
Funding
- National Institutes of Health [R01 DK60027, T32 CA09382, F32 AI62010]
- Young Chair funds
- Joslin's Diabetes and Endocrinology Research Center [P30 DK36836]
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Autoimmune regulator (Aire)-deficient mice and humans have circulating autoantibodies against a multitude of organs and multiorgan autoinflammatory infiltrates. It is not known to what extent autoantibodies or their source, B lymphocytes, are required for disease onset or progression. We show in this research that B cells must be present for Aire-deficient mice to develop fulminant infiltrates. We found no evidence that autoantibodies were directly pathogenic; rather, B cells appeared to play a critical early role in T cell priming or expansion. A therapeutic reagent directed against 8 cells, Rituximab, induced remission of the autoimmune disease in Aire-deficient mice, raising the hope of applying it to human patients with autoimmune-polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED).
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