国际检验医学杂志
國際檢驗醫學雜誌
국제검험의학잡지
INTERNATIONAL JOURNAL OF LABORATORY MEDICINE
2014年
15期
1993-1994
,共2页
鲍俊杰%邹勇%陈小红%张白杜
鮑俊傑%鄒勇%陳小紅%張白杜
포준걸%추용%진소홍%장백두
肝炎病毒 ,乙型%肝衰竭%受体
肝炎病毒 ,乙型%肝衰竭%受體
간염병독 ,을형%간쇠갈%수체
hepatitis B virus%liver falure%receptor
目的:探讨乙型肝炎病毒(HBV)相关慢加急性肝衰竭(HBV-ACLF)患者外周血自然杀伤(NK)细胞活化型受体和抑制型受体表达与肝损伤的相关性。方法利用多色流式技术检测20例 HBV-ACLF患者和20例 HBV-慢性乙型肝炎(CHB)患者外周血NK细胞活化型受体(NKP30、NKP46、NKG2D)及抑制型受体(CD158a)的表达频率。结果与 HBV-CHB患者相比,HBV-ACLF患者外周NK细胞活化型受体(NKP30、NKP46)表达均显著上调(P<0.05),而NK细胞抑制型受体CD158a的表达显著下调(P<0.05)。结论 NK细胞活化型受体NKP30和NKP46表达的增强及抑制型受体CD158a表达的减弱可能是NK细胞活化及随后 HBV-ACLF免疫介导的肝细胞损伤的重要因素。
目的:探討乙型肝炎病毒(HBV)相關慢加急性肝衰竭(HBV-ACLF)患者外週血自然殺傷(NK)細胞活化型受體和抑製型受體錶達與肝損傷的相關性。方法利用多色流式技術檢測20例 HBV-ACLF患者和20例 HBV-慢性乙型肝炎(CHB)患者外週血NK細胞活化型受體(NKP30、NKP46、NKG2D)及抑製型受體(CD158a)的錶達頻率。結果與 HBV-CHB患者相比,HBV-ACLF患者外週NK細胞活化型受體(NKP30、NKP46)錶達均顯著上調(P<0.05),而NK細胞抑製型受體CD158a的錶達顯著下調(P<0.05)。結論 NK細胞活化型受體NKP30和NKP46錶達的增彊及抑製型受體CD158a錶達的減弱可能是NK細胞活化及隨後 HBV-ACLF免疫介導的肝細胞損傷的重要因素。
목적:탐토을형간염병독(HBV)상관만가급성간쇠갈(HBV-ACLF)환자외주혈자연살상(NK)세포활화형수체화억제형수체표체여간손상적상관성。방법이용다색류식기술검측20례 HBV-ACLF환자화20례 HBV-만성을형간염(CHB)환자외주혈NK세포활화형수체(NKP30、NKP46、NKG2D)급억제형수체(CD158a)적표체빈솔。결과여 HBV-CHB환자상비,HBV-ACLF환자외주NK세포활화형수체(NKP30、NKP46)표체균현저상조(P<0.05),이NK세포억제형수체CD158a적표체현저하조(P<0.05)。결론 NK세포활화형수체NKP30화NKP46표체적증강급억제형수체CD158a표체적감약가능시NK세포활화급수후 HBV-ACLF면역개도적간세포손상적중요인소。
Objective To investigate the correlation between the expression of the activating and inhibitory receptors on periph-eral natural killer (NK) cells with the liver injury in the patients with hepatitis B virus related acute-on-chronic liver failure (HBV-ACLF) .Methods The peripheral blood samples were collected from 20 patients with HBV-ACLF and 20 patients with HBV-chro-nic hepatitis B(CHB) .The expressions of the activating receptors (NKP30 ,NKP46 ,NKG2D) and the inhibitory receptor (CD158a) on peripheral NK cells were detected by the multicolor flow cytometry .Results Compared with the HBV-CHB patients ,the ex-pression of the activating receptors NKP30 and NKP46 in the HBV-ACLF were remarkably unregulated(P<0 .05) ,but the expres-sion of the inhibitory receptor CD158a was markedly downregulated(P<0 .05) .Conclusion The enhanced expression of the activa-ting receptors NKP30 and NKP46 and the weakened expression of inhibitory receptor CD158a may be the important factor of the NK cells activation and the subsequent HBV-ACLF immune-mediated hepatocyte injury .