Th22和Th17细胞在白癜风病理机制中的作用
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摘要
目的探讨Th22和Th17细胞可能在白癜风发生发展中的作用机制。方法选择白癜风患者60例(按不同分期划分,活动期白癜风患者30例,静止期白癜风患者30例;按不同分型划分,寻常型白癜风患者29例,节段型白癜风患者31例),以年龄和性别匹配的健康正常人30例为对照。取外周静脉血,免疫荧光PCR法检测外周血中IL-22mRNA和IL-17mRNA表达,酶联免疫吸附法(ELISA)检测IL-22和IL-17表达含量。将所检测结果与白癜风患者病情进行相关分析。结果 (1)白癜风患者实验组外周血中IL-22mRNA和IL-17mRNA以及IL-22和IL-17蛋白的表达水平均明显高于健康对照组,其中活动期白癜风患者明显高于静止期患者。(2)寻常性白癜风患者外周血中IL-22mRNA和IL-17mRNA以及IL-22和IL-17表达水平显著高于节段型患者。(3)在白癜风患者组中,外周血IL-22mRNA和IL-17mRNA表达水平以及IL-22和IL-17水平呈正相关(r=0. 753,P=0. 000)。结论 Th22和Th17细胞在白癜风发生发展中起到一定作用。
Objective To explore the possible mechanisms of Th22 and Th17 cells in the pathogenesis and development of vitiligo. Methods We collected 60 cases of patients with vitiligo diseases( according to different stages,30 case of active patients,30 cases of stationary patients; according to different types,29 cases of ordinary patients and 31 cases of segmental patients). A total of 30 cases of healthy people as normal control,whose age and sex matched with patients. Peripheral venous blood was taken,and Real-Time RT-PCR was used to detect the levels of IL-22 mRNA,IL-17 mRNA,and ELISA was used to detect the levels of IL-22,IL-17.Finally,relevant analysis was made between the test results and the condition of vitiligo patients. Results In the experimental group,vitiligo patients' IL-22 mRNA IL-17 mRNA level in PBMC and IL-22,IL-17 were significantly higher than healthy controls,and the group of activity vitiligo patients was higher than vitiligo patients who were in stable stage. Ordinary vitiligo patients' IL-22 mRNA,IL-17 mRNA levels in PBMC and IL-22,IL-17 protein levels in serum were significantly higher than segmental vitiligo patients. In vitiligo patients' peripheral blood: IL-22 mRNA,IL-17 mRNA level and IL-22,IL-17 protein had significant correlation( r = 0. 753,P = 0. 000). Conclusions Th22 and Th17 cells may participate in the development of vitiligo.
Objective To explore the possible mechanisms of Th22 and Th17 cells in the pathogenesis and development of vitiligo. Methods We collected 60 cases of patients with vitiligo diseases( according to different stages,30 case of active patients,30 cases of stationary patients; according to different types,29 cases of ordinary patients and 31 cases of segmental patients). A total of 30 cases of healthy people as normal control,whose age and sex matched with patients. Peripheral venous blood was taken,and Real-Time RT-PCR was used to detect the levels of IL-22 mRNA,IL-17 mRNA,and ELISA was used to detect the levels of IL-22,IL-17.Finally,relevant analysis was made between the test results and the condition of vitiligo patients. Results In the experimental group,vitiligo patients' IL-22 mRNA IL-17 mRNA level in PBMC and IL-22,IL-17 were significantly higher than healthy controls,and the group of activity vitiligo patients was higher than vitiligo patients who were in stable stage. Ordinary vitiligo patients' IL-22 mRNA,IL-17 mRNA levels in PBMC and IL-22,IL-17 protein levels in serum were significantly higher than segmental vitiligo patients. In vitiligo patients' peripheral blood: IL-22 mRNA,IL-17 mRNA level and IL-22,IL-17 protein had significant correlation( r = 0. 753,P = 0. 000). Conclusions Th22 and Th17 cells may participate in the development of vitiligo.
引文
[1]中国中西医结合学会皮肤性病专业委员会色素病学组.白癜风临床分型及疗效标准(2003年修定稿)[J].中国中西医结合皮肤性病学杂志,2004,3(1):65.
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[6]Reimann E,Kingo K,Karelson M,et al.The mRNA expression profile of cytokines connected to the regulation of melanocyte functioning in vitiligo skin biopsy samples and peripheral blood mononuclear cells[J].Human Immunology,2012,73(4):393-398.
[7]Elela MA,Hegazy RA,Fawzy M,et al.MInterleukin 17,Interleukin22 and Fox P3 expression in tissue and ser Hm of non-segmental vitiligo:A case-controlled study on eighty-four patients[J].Eur J Dermatol,2013,23(3):350-355.
[8]Bassiouny DA,Shaker O.Role of interleukin-17 in the pathogenesis of vitiligo[J].Clinical&Experimental Dermatology,2011,36(3):292-297
[9]Kotobuki Y,Tanemura A,Yang L,et al.Dysregulation of melanocyte function by Th17-related cytokines:significance of Th17 cell infiltration in autoimmune vitiligo vulgaris[J].Pigment Cell&Melanoma Research,2012,25(2):219-230.
[10]De JA,Penacruz V,Cheng TY,et al.CD1a-autoreactive T cells are a normal component of the humanαβT cell repertoire[J].Nature Immunology,2010,11(12):1102.
[11]Ratsep R,Kingo K,Karelson M,et al.Gene expression study of IL10 family genes in vitiligo skin biopsies,peripheral blood mononuclear cells and sera[J].British Journal of Dermatology,2008,159(6):1275-1281.
[12]Wang CQ,Cruz-Inigo AE,Fuentes-Duculan J,et al.Th17 cells and activated dendritic cells are increased in vitiligo lesions[J].Plos One,2011,6(4):e18907.
[13]卢娜,许爱娥,周妙妮,等.白癜风患者白介素-17和转化生长因子-β水平的检测[J].中华皮肤科杂志,2012,45(6):433-435.
[14]Aghaei S,Sodaifi M,Jafari P,et al.DLQI scores in vitiligo:reliability and validity of the Persian version[J].BMC Dermatology,2004,4(1):8.
[15]Van GN,De LS,Vandenhaute S,et al.Different phenotypes of segmental vitiligo based on a clinical observational study[J].Journal of the European Academy of Dermatology&Venereology Jeadv,2011,25(6):673-678.
[16]Egwuagu CE.STAT3 in CD4+T helper cell differentiation and inflammatory diseases[J].Cytokine,2009,47(3):149-156.
[17]Volpe E,Servant N,Zollinger R,et al.A critical function for transforming growth factor-|[beta]|,interleukin 23 and proinflammatory cytokines in driving and modulating human TH-17 responses[J].Nature Immunology,2008,9(6):650-657.
[2]Trifari S,Kaplan CD,Tran EH,et al.Identification of a human helper T cell population that has abundant production of interleukin 22 and is distinct from TH-17,TH1 and TH2 cells[J].Nature Immunology,2009,10(8):864.
[3]El-Komy M,Amin I,Zidan A,et al.Insulin-like growth factor-1 in psoriatic plaques treated with PUVA and methotrexate[J].Journal of the European Academy of Dermatology&Venereology,2011,25(11):1288.
[4]Cai Yihua,Fleming Chris,Yan Jun.New insights of T cells in the pathoge-nesis of psoriasis[J].Cellular&Molecular Immunology,2012,9(4):302-309.
[5]Wolk K,Witte E,Witte K,et al.Biology of interleukin-22[J].Seminars in Immunopathology,2010,32(1):17-31.
[6]Reimann E,Kingo K,Karelson M,et al.The mRNA expression profile of cytokines connected to the regulation of melanocyte functioning in vitiligo skin biopsy samples and peripheral blood mononuclear cells[J].Human Immunology,2012,73(4):393-398.
[7]Elela MA,Hegazy RA,Fawzy M,et al.MInterleukin 17,Interleukin22 and Fox P3 expression in tissue and ser Hm of non-segmental vitiligo:A case-controlled study on eighty-four patients[J].Eur J Dermatol,2013,23(3):350-355.
[8]Bassiouny DA,Shaker O.Role of interleukin-17 in the pathogenesis of vitiligo[J].Clinical&Experimental Dermatology,2011,36(3):292-297
[9]Kotobuki Y,Tanemura A,Yang L,et al.Dysregulation of melanocyte function by Th17-related cytokines:significance of Th17 cell infiltration in autoimmune vitiligo vulgaris[J].Pigment Cell&Melanoma Research,2012,25(2):219-230.
[10]De JA,Penacruz V,Cheng TY,et al.CD1a-autoreactive T cells are a normal component of the humanαβT cell repertoire[J].Nature Immunology,2010,11(12):1102.
[11]Ratsep R,Kingo K,Karelson M,et al.Gene expression study of IL10 family genes in vitiligo skin biopsies,peripheral blood mononuclear cells and sera[J].British Journal of Dermatology,2008,159(6):1275-1281.
[12]Wang CQ,Cruz-Inigo AE,Fuentes-Duculan J,et al.Th17 cells and activated dendritic cells are increased in vitiligo lesions[J].Plos One,2011,6(4):e18907.
[13]卢娜,许爱娥,周妙妮,等.白癜风患者白介素-17和转化生长因子-β水平的检测[J].中华皮肤科杂志,2012,45(6):433-435.
[14]Aghaei S,Sodaifi M,Jafari P,et al.DLQI scores in vitiligo:reliability and validity of the Persian version[J].BMC Dermatology,2004,4(1):8.
[15]Van GN,De LS,Vandenhaute S,et al.Different phenotypes of segmental vitiligo based on a clinical observational study[J].Journal of the European Academy of Dermatology&Venereology Jeadv,2011,25(6):673-678.
[16]Egwuagu CE.STAT3 in CD4+T helper cell differentiation and inflammatory diseases[J].Cytokine,2009,47(3):149-156.
[17]Volpe E,Servant N,Zollinger R,et al.A critical function for transforming growth factor-|[beta]|,interleukin 23 and proinflammatory cytokines in driving and modulating human TH-17 responses[J].Nature Immunology,2008,9(6):650-657.