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糖皮质激素对重度溃疡性结肠炎患者淋巴细胞粘附分子表达的影响 被引量:17

Effect of glucocorticoid on lymphocyte adhesion molecule phenotype expression in patients with ulcerative colitis
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摘要 目的:研究糖皮质激素在分子水平抑制溃疡性结肠炎(UC)免疫反应和白细胞粘附的机制。方法:采用双标记免疫荧光染色和流式细胞仪,分析20例中重度UC患者应用泼尼松治疗前后淋巴细胞粘附分子表型的变化。结果:①中重度UC患者CD+4CD+29、CD+8CD+11a、CD+8CD+18、CD+20CD+54细胞均明显高于正常对照组(P均<0.01);好转治愈组16例治疗后上述指标明显下降;除CD+20CD+54细胞外,其余指标与正常对照组比较均无显著性差异(P均>0.05);无效恶化组4例治疗前后上述指标均无明显变化(P均>0.05),且仍明显高于正常对照组(P均<0.01)。②中重度UC患者CD+4CD+11a、CD+4CD+18细胞均较正常对照组明显降低(P均<0.01);好转治愈组治疗后均显著升高(P均<0.01),与正常对照组比较差异均无显著性(P均>0.05)。无效恶化组治疗后上述指标均无明显变化(P均>0.05),仍显著低于正常对照组(P均<0.01)。结论:糖皮质激素可能通过抑制部分淋巴细胞粘附分子的表达来抑制UC患者自体免疫过程。 Objective:To study the effect of glucocorticoid (GC) on lymphocyte adhesion molecule phenotype expression in patients with ulcerative colitis(UC).Methods:Using flow cytometric analysis and dual immunofluorescence staining method,lymphocyte adhesion molecule phenotype were examined in 20 severe UC patients before and after treatment with GC.Results:①CD+4,CD+29,CD+8CD+11a,CD+8CD+18,and CD+20CD+54 cells were much higher in UC patients than in normal controls (all P<001).After treatment with GC,they were restored to normal range in cure patients with an exception of CD+20CD+54 cells.However,no marked changes in phenotypes were found in noneffective patients following GC treatment,which were still much higher than those in normal controls (all P<001).② On the other hand,there was a significant reduction in CD+4CD+11a and CD+8CD+18 cells in UC patient compared to normal controls (both P<001),but they were markedly increased in cure patients after treatment.(P<001),and were no significant change in noneffective patients.Conclusions:GC may have beneficial effect in the treatment of UC by inhibiting the expression of lymphocyte adhesion molecule phenotype.
出处 《中国危重病急救医学》 CSCD 1998年第6期366-368,共3页 Chinese Critical Care Medicine
关键词 糖皮质激素 溃疡性结肠炎 淋巴细胞 粘附分子 glucocorticoid\ \ ulcerative colitis\ \ integrin\ \ lymphocyte adhesion molecule\ \ leukocyte functionassociated antigen
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