中国组织工程研究
中國組織工程研究
중국조직공정연구
Journal of Clinical Rehabilitative Tissue Engineering Research
2014年
38期
6222-6227
,共6页
高辉香%田玲玲%常红%朱海燕%张秋业
高輝香%田玲玲%常紅%硃海燕%張鞦業
고휘향%전령령%상홍%주해연%장추업
组织构建%组织工程%过敏性紫癜%单核细胞%Tol 样受体%MyD88%调节性T细胞%白细胞介素10%转化生长因子β
組織構建%組織工程%過敏性紫癜%單覈細胞%Tol 樣受體%MyD88%調節性T細胞%白細胞介素10%轉化生長因子β
조직구건%조직공정%과민성자전%단핵세포%Tol 양수체%MyD88%조절성T세포%백세포개소10%전화생장인자β
purpura%child%Tol-like receptors%T-lymphocytes
背景:Tol 样受体介导的信号通路转导及调节性T细胞异常活化在过敏性紫癜发病中的作用不清楚。<br> 目的:研究Tol 样受体TLR2、TLR4、TLR6在过敏性紫癜患儿外周血单核细胞的表达及调节性T细胞(Treg)的免疫应答,探讨TLR及Treg活化在敏性紫癜发病机制中的作用。<br> 方法:选择处于过敏性紫癜急性期的患儿42例为观察对象,另选取15名门诊健康查体儿童为正常对照组。采用流式细胞术检测外周血单核细胞的 TLR2、TLR4、TLR6的蛋白表达量;应用反转录-聚合酶链反应(RT-PCR)及实时荧光定量PCR检测外周血单核细胞TLR信号途径分子MyD88 mRNA的基因相对表达量;ELISA法测Treg细胞分泌的转化生长因子β、白细胞介素10的血浆水平;两组间比较采用独立样本t或t’检验,相关性分析采用Pearson相关检验。<br> 结果与结论:过敏性紫癜患儿外周血单核细胞的TLR2、TLR4、TLR6蛋白的表达及MyD88 mRNA基因的相对表达量均显著高于对照组(P <0.01);过敏性紫癜患儿血浆中转化生长因子β、白细胞介素10均高于对照组(P <0.05);过敏性紫癜患儿TLR2、TLR4、TLR6的蛋白表达量与Myd88 mRNA的基因相对表达量呈正相关(P<0.01),与血浆白细胞介素10、转化生长因子β水平无明显相关(P>0.05)。提示TLR2、TLR4、TLR6活化后可能通过MyD88依赖的途径参与敏性紫癜的发病,而过敏性紫癜急性期Treg代偿性活化可能为机体的保护性免疫应答。
揹景:Tol 樣受體介導的信號通路轉導及調節性T細胞異常活化在過敏性紫癜髮病中的作用不清楚。<br> 目的:研究Tol 樣受體TLR2、TLR4、TLR6在過敏性紫癜患兒外週血單覈細胞的錶達及調節性T細胞(Treg)的免疫應答,探討TLR及Treg活化在敏性紫癜髮病機製中的作用。<br> 方法:選擇處于過敏性紫癜急性期的患兒42例為觀察對象,另選取15名門診健康查體兒童為正常對照組。採用流式細胞術檢測外週血單覈細胞的 TLR2、TLR4、TLR6的蛋白錶達量;應用反轉錄-聚閤酶鏈反應(RT-PCR)及實時熒光定量PCR檢測外週血單覈細胞TLR信號途徑分子MyD88 mRNA的基因相對錶達量;ELISA法測Treg細胞分泌的轉化生長因子β、白細胞介素10的血漿水平;兩組間比較採用獨立樣本t或t’檢驗,相關性分析採用Pearson相關檢驗。<br> 結果與結論:過敏性紫癜患兒外週血單覈細胞的TLR2、TLR4、TLR6蛋白的錶達及MyD88 mRNA基因的相對錶達量均顯著高于對照組(P <0.01);過敏性紫癜患兒血漿中轉化生長因子β、白細胞介素10均高于對照組(P <0.05);過敏性紫癜患兒TLR2、TLR4、TLR6的蛋白錶達量與Myd88 mRNA的基因相對錶達量呈正相關(P<0.01),與血漿白細胞介素10、轉化生長因子β水平無明顯相關(P>0.05)。提示TLR2、TLR4、TLR6活化後可能通過MyD88依賴的途徑參與敏性紫癜的髮病,而過敏性紫癜急性期Treg代償性活化可能為機體的保護性免疫應答。
배경:Tol 양수체개도적신호통로전도급조절성T세포이상활화재과민성자전발병중적작용불청초。<br> 목적:연구Tol 양수체TLR2、TLR4、TLR6재과민성자전환인외주혈단핵세포적표체급조절성T세포(Treg)적면역응답,탐토TLR급Treg활화재민성자전발병궤제중적작용。<br> 방법:선택처우과민성자전급성기적환인42례위관찰대상,령선취15명문진건강사체인동위정상대조조。채용류식세포술검측외주혈단핵세포적 TLR2、TLR4、TLR6적단백표체량;응용반전록-취합매련반응(RT-PCR)급실시형광정량PCR검측외주혈단핵세포TLR신호도경분자MyD88 mRNA적기인상대표체량;ELISA법측Treg세포분비적전화생장인자β、백세포개소10적혈장수평;량조간비교채용독립양본t혹t’검험,상관성분석채용Pearson상관검험。<br> 결과여결론:과민성자전환인외주혈단핵세포적TLR2、TLR4、TLR6단백적표체급MyD88 mRNA기인적상대표체량균현저고우대조조(P <0.01);과민성자전환인혈장중전화생장인자β、백세포개소10균고우대조조(P <0.05);과민성자전환인TLR2、TLR4、TLR6적단백표체량여Myd88 mRNA적기인상대표체량정정상관(P<0.01),여혈장백세포개소10、전화생장인자β수평무명현상관(P>0.05)。제시TLR2、TLR4、TLR6활화후가능통과MyD88의뢰적도경삼여민성자전적발병,이과민성자전급성기Treg대상성활화가능위궤체적보호성면역응답。
BACKGROUND:The influence of Tol-like receptor 2 (TLR2), Tol-like receptor 4 (TLR4), Tol-like receptor 6 (TLR6) signal transduction pathway and active Treg in children with Henoch-Schonlein purpura has been unknown. <br> OBJECTIVE:To investigate the expression of TLR2, TLR4 and TLR6 in peripheral blood mononuclear cells and Treg immune response in patients with Henoch-Schonlein purpura, and to explore the role of TLR2, TLR4, TLR6 and Treg activation in the pathogenesis of Henoch-Schonlein purpura. <br> METHODForty-two hospitalized children with Henoch-Schonlein purpura were enrol ed in this study. Another 15 healthy children were selected as controls. TLR2, TLR4 and TLR6 at protein level in peripheral blood mononuclear cells were detected by flow cytometey;reverse-transcription PCR and real-time PCR were used to evaluate the level of MyD88;the levels of transforming growth factor-βand interleukin-10 were measured by enzyme-linked immunosorbent assay. t-test or t’-test was used to compare the levels of these genes and proteins. Pearson’s correlation test was done for correlation analysis. <br> RESULTS AND CONCLUSION:Compared with the control group, the protein levels of TLR2, TLR4, TLR6 and the relative expression level of MyD88 mRNA were significantly up-regulated (P<0.01). The serum levels of transforming growth factor-βand interleukin-10 were higher in the Henoch-Schonlein purpura children than the healthy children (P<0.05). There was a significant correlation between the protein levels of TLR2, TLR4, TLR6 and mRNA level of MyD88 (P<0.01), but no relationship was found between TLRs and interleukin-10, transforming growth factor-β(P>0.05). The excessive activation of TLR2, TLR4, TLR6 may be involved in the process of Henoch-Schonlein purpura via MyD88-dependent pathway, and the compensatory activation of Treg may participate in protective immunity.