Erschienen in:
01.01.2007 | Original Paper
Similar CD19 Dysregulation in Two Autoantibody-Associated Autoimmune Diseases Suggests a Shared Mechanism of B-Cell Tolerance Loss
verfasst von:
DONNA A. CULTON, MATILDA W. NICHOLAS, DONNA O. BUNCH, QUAN LI ZHEN, THOMAS B. KEPLER, MARY ANNE DOOLEY, CHANDRA MOHAN, PATRICK H. NACHMAN, STEPHEN H. CLARKE
Erschienen in:
Journal of Clinical Immunology
|
Ausgabe 1/2007
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We report here that dysregulation of CD19, a coreceptor that augments B-cell receptor (BCR) signaling, occurs at two B-cell differentiative stages in patients with systemic lupus erythematosus (SLE) and antineutrophil cytoplasmic autoantibody (ANCA) associated small vessel vasculitis (SVV). The naïve B cells of nearly all SLE and ANCA-SVV patients express ∼20% less CD19 than healthy control (HC) B cells. In contrast, a subset of memory B cells of some SLE and ANCA-SVV Pts (25–35%) express two to fourfold more CD19 than HC B cells. These CD19hi memory B cells are activated and exhibit evidence of antigen selection. Proteome array analysis of 67 autoantigens indicates that CD19hi SLE Pts exhibit a distinct autoantibody profile characterized by high levels of antibodies to small nuclear ribonucleoproteins and low levels of antiglomerular autoantibodies. These findings have implications for autoreactive B-cell activation and suggest a shared mechanism of B-cell tolerance loss in these two diseases.