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

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.

journal_name

Clin Rheumatol

journal_title

Clinical rheumatology

authors

Chen H,Zhou S,Su D,Lu L,Li X,Sun L

doi

10.1007/s10067-013-2344-x

subject

Has Abstract

pub_date

2013-12-01 00:00:00

pages

1783-90

issue

12

eissn

0770-3198

issn

1434-9949

journal_volume

32

pub_type

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