摘要目的:观察和比较先天性空肠Ⅰ型闭锁隔膜组织黏膜层内趋化因子受体6（chemokine receptor，CCR6）和巨噬细胞炎性蛋白-3α（macrophage inflammatory protein-3α，MIP-3α）的表达。方法:选用距离Treitz韧带15 cm以内的空肠Ⅰ型闭锁患儿的隔膜组织为研究组（12例），以同一患儿术中行肠切除肠吻合过程中钳取收集的正常肠壁组织为对照组（12例）。采用免疫组织化学染色法进行半定量比较两组CCR6和MIP-3α的表达差异。结果:免疫组织化学染色结果显示正常肠壁组织黏膜层内未见CCR6表达，隔膜组织黏膜层可见CCR6表达。正常肠壁组织和隔膜组织黏膜层均可见MIP-3α表达，其在隔膜组织黏膜层表达明显。半定量检测结果显示CCR6和MIP-3α分子在隔膜组织黏膜层表达增多，与正常肠壁比较，差异有统计学意义（ P=0.0027和 P=0.0130）。 结论:在胚胎发育早期，隔膜组织黏膜层高表达MIP-3α和CCR6。本研究结果提示隔膜组织黏膜层内MIP-3α通过介导CCR6对树突状细胞和效应/记忆性T淋巴细胞产生选择性趋化作用，MIP-3α和CCR6的高表达介导了树突状细胞和效应/记忆性T淋巴细胞参与肠壁自身局部免疫应答和肠闭锁隔膜组织的发生。

abstractsObjective:To explore the expressions of chemokine receptor 6 (CCR6) and macrophage inflammatory protein-3α (MIP-3α) in septum derived from type I intestinal atresia and normal intestinal wall.Methods:Septum located in intestinal wall with a distance of <15 cm from Treitz ligament and normal intestinal wall around septum from the same patients were harvested for serial tissue sectioning and subsequent immunohistochemistry staining for histological observation of both CCR6 and MIP-3α.Results:The expression of CCR6 was not detected in mucous of normal intestinal wall and it was present in septum of type I intestinal atresia. And the expression of MIP-3α was positive in mucous of both normal intestinal wall and septum of type I intestinal atresia. Semi-quantitative comparison showed that significant elevations of CCR6 and MIP-3α in mucous of septum derived from type I intestinal atresia as compared with that in normal intestinal wall ( P=0.0027 and 0.0130). Conclusion:During an early phase of fetal development, CCR6 and MIP-3α were up-regulated in mucosa of septum derived from type I intestinal atresia. And MIP-3α in septum derived from type I intestinal atresia induces chemotaxis of dendritic cell and effector/memory T lymphocyte through a up-regulation of CCR6. These pathways are probably involved in abnormal local immune response and formation of type I intestinal atresia.