Expression of TIM-1 and TIM-3 in spleen mononuclear cells and their role in Th1 polarization in primary immune thrombocytopenia patients.
- VernacularTitle:多发性骨髓瘤骨病患者成骨细胞培养及CCL3对成骨细胞作用的研究
- Author:
Xiao-Mei ZHANG
1
;
Ning-Ning SHAN
;
Yu HU
;
Xin WANG
Author Information
- Publication Type:Journal Article
- MeSH: Adolescent; Adult; Aged; Aged, 80 and over; Case-Control Studies; Female; Flow Cytometry; GATA3 Transcription Factor; metabolism; Hepatitis A Virus Cellular Receptor 1; Hepatitis A Virus Cellular Receptor 2; Humans; Male; Membrane Glycoproteins; metabolism; Membrane Proteins; metabolism; Middle Aged; Purpura, Thrombocytopenic, Idiopathic; immunology; metabolism; RNA, Messenger; genetics; Receptors, Virus; metabolism; Spleen; metabolism; Th1 Cells; immunology; Th2 Cells; immunology; Young Adult
- From: Chinese Journal of Hematology 2013;34(7):614-617
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo explore the expression and clinical significance of T cell immunoglobulin mucin (TIM)-1, TIM-3 and T cell-specific transcription factors T-bet and GATA-3 in spleen mononuclear cells in patients with primary immune thrombocytopenia (ITP).
METHODSThe spleen samples were obtained from 17 active ITP patients and 10 controls with spleen traumatic rupture. By using real-time quantitative polymerase chain reaction, the mRNA expressions of TIM-3, TIM1, T-bet and GATA-3 were studied in all subjects.
RESULTSTIM-3 mRNA levels of active ITP patients were significantly decreased to (29 ± 16)% of that of control, TIM-1 mRNA levels of active ITP patients increased to (3.20 ± 2.18) folds of that of control, but the difference was not significant. The ratio of TIM-1/ TIM-3 was elevated in active ITP patients. T-bet mRNA levels were up-regulated in ITP patients by (2.82 ± 1.57) folds (P<0.05) and the expression of GATA3 was decreased by 14% folds (P<0.05) compared to controls. The ratio of T-bet/GATA3 were significantly elevated in ITP patients.
CONCLUSIONThe imbalance between TIM-3 and TIM-1 expression might play an important role in pathogenesis of ITP.
