Erschienen in:
01.12.2013 | Original Article
High-dose methylprednisolone pulse therapy upregulated FcγRIIb expression on B cells in primary Sjögren’s syndrome patients with thrombocytopenia
verfasst von:
Haifeng Chen, Shiliang Zhou, Dinglei Su, Liwei Lu, Xia Li, Lingyun Sun
Erschienen in:
Clinical Rheumatology
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Ausgabe 12/2013
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Abstract
Abnormalities in B cell are characteristic feature of primary Sjögren’s syndrome (pSS). As FcγRIIb is a key regulator of B cells, the objective of this study is to investigate the role of the inhibitory receptor FcγRIIb in B cells from pSS patients, and whether glucocorticoid can affect B cell subpopulations or FcγRIIb expression. Thirty pSS patients and 15 healthy controls were enrolled in this study. The results showed that the percentage of memory CD19+CD27+ B cells was significantly lower in pSS patients compared to in healthy controls. FcγRIIb expression on memory CD19+CD27+ B cells from active pSS patients was significantly reduced compared with those from inactive or healthy controls. The level of FcγRIIb on memory CD19+CD27+ B cells from active pSS patients was negatively correlated with anti-SSA antibody titers and Sjögren’s syndrome disease activity index. After a high-dose methylprednisolone pulse therapy for 3 days, FcγRIIb expression on memory B cells was upregulated, with the raised level of platelets. In vitro, dexamethasone could elevate FcγRIIb expression on B cells of pSS patients in a dose-dependent manner. Taken together, our data suggest that the upregulation of FcγRIIb may be expected to be a new therapeutic strategy in pSS patients.