ROG,GATA3 and T-bet mRNA levels in peripheral blood mononuclear cells in patients with chronic hepatitis B.
- Author:
Ka ZHANG
1
;
Xin SHU
;
Hai-Fei LUO
;
Feng-Qin ZHU
;
Hong CAO
;
Qi-Huan XU
;
Gang LI
Author Information
- Publication Type:Journal Article
- MeSH: Case-Control Studies; GATA3 Transcription Factor; metabolism; Hepatitis B, Chronic; metabolism; Humans; Leukocytes, Mononuclear; metabolism; RNA, Messenger; metabolism; Real-Time Polymerase Chain Reaction; Repressor Proteins; metabolism; T-Box Domain Proteins; metabolism; Up-Regulation
- From: Journal of Southern Medical University 2016;36(2):186-189
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the role of ROG, GATA3 and T-bet in the progression of chronic hepatitis B (CHB).
METHODSThe mRNA levels of ROG, GATA3 and T-bet in peripheral blood mononuclear cells (PBMCs) from 135 patients with CHB (including 45 mild cases, 42 moderate cases, and 48 severe cases) and 15 healthy control subjects were detected by real-time quantitative PCR.
RESULTSThe levels of T-bet mRNA in the PBMCs were significantly higher in CHB patients than in the healthy controls (P<0.05), and also differed significantly between the 3 groups of CHB patients (P<0.05). ROG mRNA levels were significantly higher in severe cases of CHB than in the healthy controls and mild and moderate CHB cases (P<0.05), but were similar among the latter 3 groups (P>0.05). The mRNA level of GATA3 in the PBMCs were significantly higher in moderate and severe CHB cases than in the healthy controls and mild CHB cases (P<0.05). The T-bet/GATA3 ratio was significantly greater in the 3 CHB groups than in the control group (P<0.05) but comparable between the 3 CHB groups (P>0.05). ROG levels were not correlated with GATA3 levels or T-bet/GATA3 ratio in the CHB cases.
CONCLUSIONSThe mRNA levels of ROG, GATA3 and T-bet in the PBMCs are obviously up-regulated in CHB patients and these 3 genes may participate in the progression of CHB. ROG plays an important role in correcting and maintaining the new balance of Th1/Th2.
