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Dexamethasone inhibits immunoreactivity of dendritic cells in patients with chronic idiopathic thrombocytopenic purpura.

Authors: Chu, XX  Huang, BH  Zhang, XL  Chen, LM  Wang, Y  Yu, WJ  Wang, XL  Qin, YP 
Citation: Chu XX, etal., Blood Coagul Fibrinolysis. 2010 Sep;21(6):564-7. doi: 10.1097/MBC.0b013e32833c2b8c.
Pubmed: (View Article at PubMed) PMID:20581660
DOI: Full-text: DOI:10.1097/MBC.0b013e32833c2b8c

The objective of this study was to investigate the possible effects of dexamethasone treatment on the immunoreactivity of dendritic cells in patients with chronic idiopathic thrombocytopenic purpura (ITP). Thirty-six newly diagnosed patients with chronic ITP received an oral high dose of dexamethasone (HD-DXM) at single daily doses of 40 mg for 4 consecutive days. The CD14 leukocytes isolated from the 21 remission patients and 10 normal controls were stimulated by recombinant human granulocyte-macrophage colony-stimulating factor and rhIL-4. The surface antigens of the dendritic cells were analyzed by flow cytometry and the level of IL-12p70 in the supernatant was detected by enzyme-linked immunosorbent assay. In ITP patients, the expression of both CD80 and CD86 in dendritic cells were significantly increased compared with those of the normal controls (51.60 +/- 13.47 vs. 36.03 +/- 15.43%, 61.50 +/- 15.93 vs. 40.28 +/- 11.49%, respectively; P < 0.05). After HD-DXM treatment, both CD80 and CD86 were decreased to levels comparable to normal controls (P > 0.05). The level of IL-12p70 in ITP patients was significantly higher (67.52 +/- 14.43 pg/ml) than the controls (39.78 +/- 10.03 pg/ml, P < 0.05). After treatment, IL-12p70 was reduced to 43.90 +/- 8.49 pg/ml with no significant differences between ITP group and control (P > 0.05). Dendritic cells and their cytokine secretion play important roles in ITP, and DXM may achieve its therapeutic effect on ITP by inhibiting immune responses through suppressing the function of dendritic cells.


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RGD Object Information
RGD ID: 11520785
Created: 2016-08-03
Species: All species
Last Modified: 2016-08-03
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.