High-dose methylprednisolone pulse therapy upregulated FcγRIIb expression on B cells in primary Sjögren's syndrome patients with thrombocytopenia.
Clin Rheumatol
; 32(12): 1783-90, 2013 Dec.
Article
en En
| MEDLINE
| ID: mdl-23917390
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.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Trombocitopenia
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Metilprednisolona
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Linfocitos B
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Síndrome de Sjögren
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Receptores de IgG
Tipo de estudio:
Observational_studies
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Risk_factors_studies
Límite:
Adult
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Female
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Humans
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Male
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Middle aged
Idioma:
En
Revista:
Clin Rheumatol
Año:
2013
Tipo del documento:
Article
Pais de publicación:
Alemania