The role of interleukin-18 and interleukin-18 receptor in predominant Th1 immune response of patients with immune thrombocytopenia.
- Author:
Qian WANG
1
;
Xiao-Jing YANG
;
Ning-Ning SHAN
;
Ming HOU
;
Xue-Bin JI
;
Chun-Yan WANG
;
Xiao-Juan ZHU
;
Lei YANG
;
Xiao-Lin ZHANG
;
Jun PENG
;
Dao-Xin MA
;
Yan SHI
Author Information
- Publication Type:Journal Article
- MeSH: Adolescent; Adult; Aged; Case-Control Studies; Female; GATA3 Transcription Factor; metabolism; Humans; Interleukin-18; immunology; metabolism; Male; Middle Aged; Purpura, Thrombocytopenic, Idiopathic; immunology; metabolism; Receptors, Interleukin-18; immunology; metabolism; T-Box Domain Proteins; metabolism; Th1 Cells; immunology; metabolism; Young Adult
- From: Chinese Journal of Hematology 2009;30(10):658-661
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo evaluate the role of interleukin (IL)-18 and IL-18 receptor (IL-18R) in the predominant Th1 type cytokine response in patients with immune thrombocytopenia (ITP).
METHODSFifteen patients with active phase ITP, eighteen in remission and thirteen healthy controls were enrolled in this study. T-bet and GATA-3 mRNA levels in peripheral blood mononucleated cells (PBMNC) were measured by reverse transcriptase polymerase chain reaction (RT-PCR); the plasma IL-18 level by enzyme linked immunosorbent assay (ELISA), the expression of IL-18R on CD3(+) lymphocytes and total lymphocytes by flow cytometry(FCM).
RESULTSThe T-bet mRNA levels in patients with active phase ITP was 3.572 fold as much as that in the controls (P < 0.05), while the GATA-3 mRNA levels were 0.378 fold of that in controls (P < 0.05). The levels of plasma IL-18 and IL-18R on CD3(+) lymphocytes were significantly increased in active phase ITP than in remission phase and controls. There was no difference in ratio of T-bet/GATA-3 between remitted ITP and controls and so was for T-bet mRNA, GATA-3 mRNA, plasma IL-18 and IL-18R on CD3(+) lymphocytes.
CONCLUSIONITP as a disease of Th1-dominant response there is an unbalance between T-bet and GATA-3 in its active phase; IL-18 and IL-18R being upregulated.
