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SAT0170 Decreased expression of FCΓRIIB on B cells from primary sjögren’s syndrome patients
  1. S. Zhou,
  2. X. Li,
  3. L. Sun
  1. The Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing, China

Abstract

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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