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B cell maturation and its dysregulation in autoimmunity
Author(s) -
Lu Liwei
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1073.19
Subject(s) - b cell activating factor , autoimmunity , immunology , autoantibody , cytokine , medicine , rheumatoid arthritis , pathogenesis , arthritis , autoimmune disease , tumor necrosis factor alpha , antibody , b cell
B cell activating factor (BAFF), a member of TNF family cytokines, has been shown to enhance B cell maturation and survival. Although increased serum levels of BAFF has been observed in patients with rheumatoid arthritis, the role of BAFF in the disease pathogenesis remains not fully understood. Both plasma cells (PCs) and the cytokine IL‐17 are known to promote autoimmune arthritis but whether BAFF regulates Th17 production and its involvement in autoantibody‐producing PC generation are not clear. We administered recombinant BAFF intravenously into type II collagen (CII)‐induced arthritis (CIA) mice. Increased severity of the disease as evaluated by elevated clinical scores was observed in BAFF‐treated CIA mice, which was accompanied by increased serum levels of CII‐specific antibody. Flow cytometric analysis showed an expansion of peripheral B compartment in BAFF‐treated CIA mice with significantly increased IL‐17 production. Immunohistochemical studies revealed a greater accumulation of CD138+ PCs and IL‐17+ cells with more pronounced cartilage damage and bone erosion in the joints of BAFF‐treated CIA mice. Our findings show that BAFF enhances the generation of IL‐17+ cells and CII‐specific PCs in the CIA mice, suggesting a pathogenic role for BAFF in the development of autoimmune arthritis.