Background Abnormalities in B cell are characteristic features of primary Sjögren’s syndrome (pSS). FcγRIIb (CD32b), an inhibitory receptor on B cells, is a key regulator of B cells and might be expected to be involved in the pathogenesis of autoimmune diseases.
Objectives This work was carried out to evaluate the expression of FcγRIIb on B cells from pSS patients, and the influence of high-dose methylprednisolone (HD-MP) pulse therapy.
Methods FcγRIIb expression on peripheral B cells from 19 pSS patients and 15 healthy controls was examined by flow cytometry (FACS). The levels of serum ant-SSA and SSB antibodies were determined using enzyme-linked immunosorbent assay (ELISA). Five patients who suffered from serious thrombocytopenia and underwent a three-day high-dose methylprednisolone pulse therapy were further assessed for FcγRIIb changes on their B cells
Results The percentages of memory CD19+CD27+ B cell subpopulation were significantly lower in pSS patients compared to normal controls (p<0.01). The expression of FcγRIIb in active pSS memory CD19+CD27+ B cells was significantly reduced than that in both inactive (p<0.01) and normal controls (p<0.001). pSS patients in serum ant-SSA/SSB antibodies positive group displayed a decreased expression of FcγRIIb on memory CD19+CD27+ B cell compared to those patients with serum negative ant-SSA/SSB antibodies (both p<0.01).The expression of FcγRIIb memory CD19+CD27+ B cells was inversely correlated with anti-SSA antibody titers in active pSS. After a three-day high-dose methylprednisolone pulse therapy, the expression of FcγRIIb on B cells was almost normalized, especially on memory B cells, meanwhile with raised number of platelet.
Conclusions There is a reduced expression of FcγRIIb on peripheral memory B cells from active pSS patients, which is inversely associated with ant-SSA/SSB antibodies levels. Decreased expression of FcγRIIb might play an important role in the pathogenesis of pSS. HD-MP could induce FcγRIIb expression on B cells from pSS. The upregulation of FcγRIIb is expected as a new therapeutic strategy in pSS.
Disclosure of Interest None Declared
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