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作 者:师锁柱[1] 陈香美[1] 李建军[1] 张雪光[1] 尹忠[1] 朱飞[1] 吴曼[1] 詹俊[1]
机构地区:[1]解放军总医院肾脏科,全军肾脏病研究所暨重点实验室,北京100853
出 处:《临床与实验病理学杂志》2007年第2期175-177,共3页Chinese Journal of Clinical and Experimental Pathology
基 金:国家自然基金"创新研究群体"项目(30121005)
摘 要:目的探讨巨噬细胞移动抑制因子(MIF)在非IgA系膜增生性肾小球肾炎患者肾组织中的表达及其意义。方法应用免疫组织化学双标记技术检测正常对照组及不同病变程度非IgA系膜增生性肾小球肾炎患者肾组织内MIF和人巨噬细胞标记抗原CD68的表达。结果在正常对照组和IgA系膜增生性肾小球肾炎患者轻度组仅有少量MIF和CD68表达。随着非IgA系膜增生性肾小球肾炎病变程度的加重,MIF、CD68的表达逐渐增强,重度病变时,MIF、CD68的表达最强,且MIF表达水平与CD68表达呈正相关(r=0.87,P<0.01)。结论肾组织内MIF表达上调所导致的巨噬细胞浸润增加可能是非IgA系膜增生性肾小球肾炎进展的重要机制之一。Purpose To explore the expression and significance of macrophage migration inhibitory factor (MIF) in the kidney of patients with non-IgA mesangial proliferative glomerulonephritis (MsPGN). Methods MIF protein expression and the marker of human maerophage ( CD68 ) in renal tissue of non-IgA MsPGN were detected with a double labeling immunostaining method. Results Weak expression of MIF and CD68 was found in normal control and mild groups, and with the advancement of the disease, the expression of MIF and CD68 was gradually increased. Among all the groups, the expression of MIF and CD68 was the strongest in severe groups, and the expression of MIF was correlated with that of CD68. Conclusions It may be an important mechanism for the progression of non- IgA MsPGN that upregulation of MIF can enhance infiltration of macrophages.
关 键 词:巨噬细胞移动抑制因子 非IGA系膜增生性肾小球肾炎 CD68
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