ArticleClinical rheumatology2013
High-dose methylprednisolone pulse therapy upregulated FcγRIIb expression on B cells in primary Sjögren's syndrome patients with thrombocytopenia.
Article in Clinical rheumatology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Systems serology identifies FcR-related autoantibody signatures and functions for Sjögren's syndrome.EMBO molecular medicine · 2026Article
- Primary Sjögren's syndrome-associated immune thrombocytopenia: from pathogenesis to treatment.Frontiers in immunology · 2026Review
- Eltrombopag for the treatment of refractory connective tissue disease-related thrombocytopenia: a pilot study of 52 cases.Arthritis research & therapy · 2025Observational
- Clinical and laboratory features of primary Sjögren's syndrome complicated with mild to severe thrombocytopenia.Annals of translational medicine · 2022Article
- Clinical profiles of SS-ILD compared with SS-NILD in a Chinese population: a retrospective analysis of 735 patients.Annals of medicine · 2021Article
- Activation of Toll-Like Receptor 7 Signaling Pathway in Primary Sjögren's Syndrome-Associated Thrombocytopenia.Frontiers in immunology · 2021Article
- Clinical Characteristics of Secondary Immune Thrombocytopenia Associated With Primary Sjögren's Syndrome.Frontiers in medicine · 2020Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
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.
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