中华临床医师杂志(电子版)
中華臨床醫師雜誌(電子版)
중화림상의사잡지(전자판)
CHINESE JOURNAL OF CLINICIANS(ELECTRONIC VERSION)
2014年
21期
3789-3794
,共6页
訾广芹%付元%陈秀霞%曹永献%张庆群%常红
訾廣芹%付元%陳秀霞%曹永獻%張慶群%常紅
자엄근%부원%진수하%조영헌%장경군%상홍
紫癜,过敏性%Toll样受体6%干扰素Ⅱ型%白细胞介素4%白细胞介素17
紫癜,過敏性%Toll樣受體6%榦擾素Ⅱ型%白細胞介素4%白細胞介素17
자전,과민성%Toll양수체6%간우소Ⅱ형%백세포개소4%백세포개소17
Purpura,Schoenlein-Henoch%Toll-like receptor 6%Interferon type Ⅱ%Interleukin-4%Interleukin-17
目的:探讨TLR6在过敏性紫癜(HSP)患儿外周血单个核细胞(PBMC)的表达及其与Th1、Th2和Th17细胞免疫应答的相关性,探讨TLR6与HSP发病机制的关系。方法选取我院住院的急性期HSP患儿42例为研究对象,另选取健康儿童30例作为正常对照组。采用流式细胞术检测外周血单个核细胞TLR6蛋白表达,实时荧光定量PCR技术检测外周血单个核细胞MyD88 mRNA的基因相对表达量,ELISA法检测血浆IFN-γ、IL-4、IL-17水平。结果(1)HSP患儿外周血单个核细胞TLR6蛋白表达(TLR6阳性细胞百分率及平均荧光强度)显著高于正常对照组(t'=9.40, P<0.01;t'=10.49,P<0.01),HSP组外周血单个核细胞MyD88 mRNA相对表达量显著明显高于正常对照组(t'=2.46,P<0.01)。(2)HSP组血浆IL-4水平显著高于对照组(t'=3.44,P<0.01),IFN-γ水平高于对照组(t'=2.44,P<0.05),IFN-γ/IL-4比值低于对照组(t'=2.27,P<0.05),IL-17水平显著高于对照组(t'=2.64,P<0.01)。(3)HSP组单个核细胞TLR6蛋白表达与MyD88 mRNA呈显著正相关(r=0.79;P<0.01);与血浆IL-4水平呈显著正相关(r=0.69,P<0.01);与IFN-γ/IL-4比值呈负相关(r=-0.38,P<0.05);与IL-17水平呈正相关(r=0.36,P<0.05);与血浆IFN-γ水平不存在相关性(P>0.05)。结论 TLR6活化可能参与了HSP的免疫发病机制;HSP患儿体内存在Th1/Th2失衡,Th17异常活化,活化的TLR6可能通过上调Th2、Th17免疫应答介导HSP的免疫发病机制。
目的:探討TLR6在過敏性紫癜(HSP)患兒外週血單箇覈細胞(PBMC)的錶達及其與Th1、Th2和Th17細胞免疫應答的相關性,探討TLR6與HSP髮病機製的關繫。方法選取我院住院的急性期HSP患兒42例為研究對象,另選取健康兒童30例作為正常對照組。採用流式細胞術檢測外週血單箇覈細胞TLR6蛋白錶達,實時熒光定量PCR技術檢測外週血單箇覈細胞MyD88 mRNA的基因相對錶達量,ELISA法檢測血漿IFN-γ、IL-4、IL-17水平。結果(1)HSP患兒外週血單箇覈細胞TLR6蛋白錶達(TLR6暘性細胞百分率及平均熒光彊度)顯著高于正常對照組(t'=9.40, P<0.01;t'=10.49,P<0.01),HSP組外週血單箇覈細胞MyD88 mRNA相對錶達量顯著明顯高于正常對照組(t'=2.46,P<0.01)。(2)HSP組血漿IL-4水平顯著高于對照組(t'=3.44,P<0.01),IFN-γ水平高于對照組(t'=2.44,P<0.05),IFN-γ/IL-4比值低于對照組(t'=2.27,P<0.05),IL-17水平顯著高于對照組(t'=2.64,P<0.01)。(3)HSP組單箇覈細胞TLR6蛋白錶達與MyD88 mRNA呈顯著正相關(r=0.79;P<0.01);與血漿IL-4水平呈顯著正相關(r=0.69,P<0.01);與IFN-γ/IL-4比值呈負相關(r=-0.38,P<0.05);與IL-17水平呈正相關(r=0.36,P<0.05);與血漿IFN-γ水平不存在相關性(P>0.05)。結論 TLR6活化可能參與瞭HSP的免疫髮病機製;HSP患兒體內存在Th1/Th2失衡,Th17異常活化,活化的TLR6可能通過上調Th2、Th17免疫應答介導HSP的免疫髮病機製。
목적:탐토TLR6재과민성자전(HSP)환인외주혈단개핵세포(PBMC)적표체급기여Th1、Th2화Th17세포면역응답적상관성,탐토TLR6여HSP발병궤제적관계。방법선취아원주원적급성기HSP환인42례위연구대상,령선취건강인동30례작위정상대조조。채용류식세포술검측외주혈단개핵세포TLR6단백표체,실시형광정량PCR기술검측외주혈단개핵세포MyD88 mRNA적기인상대표체량,ELISA법검측혈장IFN-γ、IL-4、IL-17수평。결과(1)HSP환인외주혈단개핵세포TLR6단백표체(TLR6양성세포백분솔급평균형광강도)현저고우정상대조조(t'=9.40, P<0.01;t'=10.49,P<0.01),HSP조외주혈단개핵세포MyD88 mRNA상대표체량현저명현고우정상대조조(t'=2.46,P<0.01)。(2)HSP조혈장IL-4수평현저고우대조조(t'=3.44,P<0.01),IFN-γ수평고우대조조(t'=2.44,P<0.05),IFN-γ/IL-4비치저우대조조(t'=2.27,P<0.05),IL-17수평현저고우대조조(t'=2.64,P<0.01)。(3)HSP조단개핵세포TLR6단백표체여MyD88 mRNA정현저정상관(r=0.79;P<0.01);여혈장IL-4수평정현저정상관(r=0.69,P<0.01);여IFN-γ/IL-4비치정부상관(r=-0.38,P<0.05);여IL-17수평정정상관(r=0.36,P<0.05);여혈장IFN-γ수평불존재상관성(P>0.05)。결론 TLR6활화가능삼여료HSP적면역발병궤제;HSP환인체내존재Th1/Th2실형,Th17이상활화,활화적TLR6가능통과상조Th2、Th17면역응답개도HSP적면역발병궤제。
Objective To investigate the expression of TLR6 in peripheral blood mononuclear cells and its correlation with Th1, Th2 and Th17 immune response in children with Henoch-Schonlein purpura(HSP), to explore the relationship between Toll-like receptor 6 and the pathogenesis of HSP. Methods Forty-two patients with HSP and 30 age-matched healthy subjects were recruited. Flow cytometry (FCM) was performed to detect the expression of TLR6. The relative expression level of MyD88 mRNA in PBMCs was detected by real-time fluorescent PCR. The levels of IFN-γ, IL-4 and IL-17 in plasma were determined by ELISA. Results (1)The levels of TLR6 and MyD88 mRNA of the HSP children were significantly higher than the control group (P<0.01). (2)The levels of IL-4, IFN-γand IL-17 in plasma of HSP children were significantly higher than the controls (t'=3.44, P<0.01; t'=2.44, P<0.05;t'=2.64, P<0.01), and the ratio of IFN-γ/IL-4 in plasma of HSP children was lower than the control group (t'=2.27, P<0.05). (3)The mRNA expression of MyD88 showed a positive correlation with expression of Toll-like receptor 6 protein of CD4+T in HSP children (r=0.79; P<0.01); Toll-like receptor 6 had positively correlated with IL-4 (r=0.69, P<0.01); and negatively correlated with the ratio of IFN-γ/IL-4 ratio (r=-0.38, P<0.05); and positively associated with IL-17 (r=0.36, P<0.05); had no correlation with plasma IFN-γ (P>0.05). Conclusion The aberrant activation of TLR6 might be associated with the immunological pathogenesis of HSP by enhancing Th17 immune response. The hyper-activation of Th2 and Th17 might be involved in the process of HSP development.