中华内科杂志
中華內科雜誌
중화내과잡지
CHINESE JOURNAL OF INTERNAL MEDICINE
2012年
8期
634-637
,共4页
张翔%冯建明%李文倩%李建平%陈绍斌%韩国雄
張翔%馮建明%李文倩%李建平%陳紹斌%韓國雄
장상%풍건명%리문천%리건평%진소빈%한국웅
干扰素Ⅱ型%紫癜,血小板减少性,免疫性%CXC亚族趋化因子受体3%I-TAC
榦擾素Ⅱ型%紫癜,血小闆減少性,免疫性%CXC亞族趨化因子受體3%I-TAC
간우소Ⅱ형%자전,혈소판감소성,면역성%CXC아족추화인자수체3%I-TAC
Interferon type Ⅱ%Purpura,thrombocytopenic,immune%CXCR3%I-TAC
目的 探讨CXC亚族趋化因子受体3(CXCR3)及其配体I-TAC在免疫性血小板减少性紫癜(ITP)发病机制中的作用.方法 应用ELISA和逆转录PCR,对30例初诊及复发ITP患者治疗前、18例治疗后缓解患者和24例健康人的血浆IFNγ、I-TAC和外周血单个核细胞(PBMNC)中CXCR3进行检测.结果 治疗前ITP患者血浆中IFNγ的含量明显高于治疗后组与正常对照组[ (71.45±17.62) ng/L比(36.94±14.86) ng/L和(25.28±12.85) ng/L,P<0.05],ITP治疗后血浆IFNγ的含量仍高于正常对照组(P<0.05).治疗前ITP患者血浆中I-TAC的含量与治疗后及正常对照组相比,3组之间差异无统计学意义[( 455.56±144.70) ng/L比(488.24±164.70) ng/L和(382.97±167.43) ng/L,P>0.05].与正常对照组相比,治疗前与治疗后组ITP患者PBMNC高表达CXCR3 mRNA[6.76(3.03,37.00),1.76(0.45,14.18)比0.12(0.04,0.28),P<0.05],治疗后CXCR3表达降低,但与治疗前相比差异无统计学意义(P>0.05).结论 ITP患者高表达Th1细胞因子,同时CXCR3+细胞可能通过趋化机制在ITP免疫机制中发挥一定的作用.
目的 探討CXC亞族趨化因子受體3(CXCR3)及其配體I-TAC在免疫性血小闆減少性紫癜(ITP)髮病機製中的作用.方法 應用ELISA和逆轉錄PCR,對30例初診及複髮ITP患者治療前、18例治療後緩解患者和24例健康人的血漿IFNγ、I-TAC和外週血單箇覈細胞(PBMNC)中CXCR3進行檢測.結果 治療前ITP患者血漿中IFNγ的含量明顯高于治療後組與正常對照組[ (71.45±17.62) ng/L比(36.94±14.86) ng/L和(25.28±12.85) ng/L,P<0.05],ITP治療後血漿IFNγ的含量仍高于正常對照組(P<0.05).治療前ITP患者血漿中I-TAC的含量與治療後及正常對照組相比,3組之間差異無統計學意義[( 455.56±144.70) ng/L比(488.24±164.70) ng/L和(382.97±167.43) ng/L,P>0.05].與正常對照組相比,治療前與治療後組ITP患者PBMNC高錶達CXCR3 mRNA[6.76(3.03,37.00),1.76(0.45,14.18)比0.12(0.04,0.28),P<0.05],治療後CXCR3錶達降低,但與治療前相比差異無統計學意義(P>0.05).結論 ITP患者高錶達Th1細胞因子,同時CXCR3+細胞可能通過趨化機製在ITP免疫機製中髮揮一定的作用.
목적 탐토CXC아족추화인자수체3(CXCR3)급기배체I-TAC재면역성혈소판감소성자전(ITP)발병궤제중적작용.방법 응용ELISA화역전록PCR,대30례초진급복발ITP환자치료전、18례치료후완해환자화24례건강인적혈장IFNγ、I-TAC화외주혈단개핵세포(PBMNC)중CXCR3진행검측.결과 치료전ITP환자혈장중IFNγ적함량명현고우치료후조여정상대조조[ (71.45±17.62) ng/L비(36.94±14.86) ng/L화(25.28±12.85) ng/L,P<0.05],ITP치료후혈장IFNγ적함량잉고우정상대조조(P<0.05).치료전ITP환자혈장중I-TAC적함량여치료후급정상대조조상비,3조지간차이무통계학의의[( 455.56±144.70) ng/L비(488.24±164.70) ng/L화(382.97±167.43) ng/L,P>0.05].여정상대조조상비,치료전여치료후조ITP환자PBMNC고표체CXCR3 mRNA[6.76(3.03,37.00),1.76(0.45,14.18)비0.12(0.04,0.28),P<0.05],치료후CXCR3표체강저,단여치료전상비차이무통계학의의(P>0.05).결론 ITP환자고표체Th1세포인자,동시CXCR3+세포가능통과추화궤제재ITP면역궤제중발휘일정적작용.
Objective To investigate the roles of the chemokine receptor CXCR3 and its ligand I-TAC in the pathogenesis of immune thrombocytopenic purpura (ITP).Methods A total of 48 ITP patients were enrolled in this study:30 with newly diagnosed or relapse ITP and 18 in remission after treatment,and 24 healthy volunteers were as controls.IFNγ and I-TAC in plasma were detected by ELISA.The mRNA expression of CXCR3 in the peripheral blood mononuclear cells (PBMNCs) was determined by quantitative RT-PCR.Results The IFNγ level in the plasma of ITP patients before the treatment was obviously increased than those in the remission group and controls[ (71.45 ± 17.62)ng/L vs (36.94 ±14.86 )ng/L and (25.28 ± 12.85 )ng/L,all P < 0.05 ]and those in the remission group was higher than in the controls ( P < 0.05 ).In contrast,there were no statistic differences of the levels of I-TAC among the three groups[ (455.56 ± 144.70 ) ng/L,( 488.24 ± 164.70 ) ng/L and ( 382.97 ± 167.43 ) ng/L,P >0.05 ].Both ITP patients before the treatment and remission groups expressed more CXCR3 mRNA [ 6.76(3.03,37.00),1.76 (0.45,14.18 ) vs 0.12 ( 0.04,0.28 ),P < 0.05 ].After effective therapy,CXCR3mRNA expression decreased,while it was still higher than that in the controls.Conclusions Our data demonstrate that Th1 cytokine (IFNγ) dominance is reflected in ITP.Simultaneously,the CXCR3 + cell may play a role in cell-mediated immunity through chemotaxis in ITP.