High-dose methylprednisolone pulse therapy upregulated FcγRIIb expression on B cells in primary Sjogren's syndrome patients with thrombocytopenia

Abnormalities in B cell are characteristic feature of primary Sjogren's syndrome (pSS). As Fc gamma RIIb is a key regulator of B cells, the objective of this study is to investigate the role of the inhibitory receptor Fc gamma RIIb in B cells from pSS patients, and whether glucocorticoid can affect B cell subpopulations or Fc gamma RIIb 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. Fc gamma RIIb 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 Fc gamma RIIb on memory CD19(+)CD27(+) B cells from active pSS patients was negatively correlated with anti-SSA antibody titers and Sjogren's syndrome disease activity index. After a high-dose methylprednisolone pulse therapy for 3 days, Fc gamma RIIb expression on memory B cells was upregulated, with the raised level of platelets. In vitro, dexamethasone could elevate Fc gamma RIIb expression on B cells of pSS patients in a dose-dependent manner. Taken together, our data suggest that the upregulation of Fc gamma RIIb may be expected to be a new therapeutic strategy in pSS patients.