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High-dose dexamethasone shifts the balance of stimulatory and inhibitory Fcgamma receptors on monocytes in patients with primary immune thrombocytopenia.

Authors: Liu, XG  Ma, SH  Sun, JZ  Ren, J  Shi, Y  Sun, L  Dong, XY  Qin, P  Guo, CS  Hou, M  Peng, J 
Citation: Liu XG, etal., Blood. 2011 Feb 10;117(6):2061-9. doi: 10.1182/blood-2010-07-295477. Epub 2010 Dec 3.
Pubmed: (View Article at PubMed) PMID:21131591
DOI: Full-text: DOI:10.1182/blood-2010-07-295477

The human Fcgamma receptor (FcgammaR) system is composed of 2 opposing families, the activating FcgammaRs (FcgammaRI, FcgammaRIIa, and FcgammaRIII) and the inhibitory FcgammaR (FcgammaRIIb). The disturbed balance of the activating and inhibitory FcgammaRs has been implicated in the pathogenesis of many autoimmune diseases. In this study, the expression of FcgammaRs on monocytes was determined in 23 patients with primary immune thrombocytopenia (ITP) before and after high-dose dexamethasone (HD-DXM) treatment. The FcgammaRI expression was significantly higher in ITP patients and decreased after HD-DXM treatment. The ratio of FcgammaRIIa/IIb mRNA expression on monocytes was significantly higher in untreated patients than in healthy controls. After HD-DXM therapy, the ratio decreased and the increased expression of FcgammaRIIb mRNA and protein coincided with a remarkable decrease in the expression of FcgammaRIIa, FcgammaRI, and monocyte phagocytic capacity. There was no significant difference in FcgammaRIII expression on monocytes between patients and controls. In vitro cell-culture experiments showed that DXM could induce FcgammaRIIa and FcgammaRIIb expression in monocytes from ITP patients, with FcgammaRIIb at higher amplitudes. These findings suggested that the disturbed FcgammaR balance might play a role in the pathogenesis of ITP, and that HD-DXM therapy could shift monocyte FcgammaR balance toward the inhibitory FcgammaRIIb in patients with ITP.

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CRRD Object Information
CRRD ID: 11040933
Created: 2016-03-17
Species: All species
Last Modified: 2016-03-17
Status: ACTIVE



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