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溃疡性结肠炎患者外周血和肠道黏膜辅助性T细胞表型分析 被引量:2

Phenotypic analysis of Th cells in colonic mucosa and peripheral blood of patients with ulcerative colitis
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摘要 目的探讨Th细胞各亚群比例在溃疡性结肠炎(UC)发病中的变化及意义。方法按照2007年济南标准收集UC患者20例,对照组16例。利用细胞内细胞因子染色和四色荧光抗体流式细胞术对肠黏膜及外周血淋巴细胞作表型分析,比较各组肠黏膜固有层单个核细胞(cLPMC)和外周血单个核细胞(PBMC)中Th1、Th2、Th17细胞比例的改变。结果UC组cLPMC中Th17细胞比例较对照组升高,分别为3.75%(6.93%)和1.25%(3.70%),在PBMC中为1.40%(2.15%)和0.70%(0.33%),两组间差异均有统计学意义(P值均〈0.05)。UC患者cLPMC中TE17细胞比例与疾病评分呈正相关(r=0.34,P〈0.05)。UC组和对照组Th1、Th2细胞在cLPMC和PBMC中的比例均差异无统计学意义(P〉0.05),且不同疾病活动度患者间差异亦无统计学意义(P值均〉0.05)。结论在Th细胞各亚群中,Th17细胞是介导UC肠道局部和外周免疫应答的优势细胞,可能成为UC治疗的有效靶点。 Objective To analyze the changes of proportion of Th1/Th2/Th17 cells in colonic mucosa and peripheral blood in pathogenesis of ulcerative colitis (UC) and its significance. Methods Twenty patients with UC were enrolled according to the criterion established in Jinan in 2007 and 16 patients were served as controls. The phenotypes of the colonic mucosa and peripheral blood were analysis by using flow cytometry. The variation of proportion of Th1/Th2/Th17 in colonic lamina propria mononuclear cells (cLPMCs) and peripheral blood mononuclear cells (PBMCs) were compared between two groups. Results The proportion of Th17 cell in cLPMCs was increased in UC group compared with controls [3.75% (6.93%)vs. 1.25% (3.70%), P〈0. 05], whereas it was 1.40% (2.15%) in UC group and 0. 70%(0. 33%) in controls in PBMCs with significant difference (P 〈0.05). The proportion of Th17 cell in cLPMCs was positively correlated with clinical parameters of the disease (r= 0.34, P〈0.05). No difference was found in proportion of Th1 or Th2 cells in cLPMCs or PBMCs between UC group and controls. Conclusions Among three helper T cells, Th17 cell in UC patients is predominant both in colonic mucosa and peripheral blood, which can be used as an effective target for treatment.
出处 《中华消化杂志》 CAS CSCD 北大核心 2009年第9期537-539,共3页 Chinese Journal of Digestion
基金 国家自然科学基金资助项目(30770986)
关键词 结肠炎 溃疡性 T淋巴细胞 辅助诱导 白细胞介素-17 Colitis, ulcerative T lymphocytes, Helper inducer lnterleukin-17
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