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婴儿猝死综合征受害者细支气管中树突状细胞的增殖。

Proliferation of dendritic cells in the bronchioles of sudden infant death syndrome victims.

作者信息

Haque A K, Mancuso M G

机构信息

Department of Pathology, University of Texas Medical Branch, Galveston.

出版信息

Mod Pathol. 1993 May;6(3):360-70.

PMID:8346185
Abstract

Sudden Infant Death Syndrome (SIDS) victims have significantly thickened bronchiolar walls with increased mononuclear cells in the adventitia. An immunohistochemical study was performed on 25 SIDS and 18 aged-matched control infants to characterize these cells. The panel of antibodies included alpha-1-antitrypsin, lysozyme, actin, vimentin, Leu M1, NSE, S-100, Leu 6, bombesin, serotonin, anti-substance P, vasoactive intestinal peptide, MAC 387, and Factor XIIIa. The bronchiolar cells stained with S-100 antibody and demonstrated slender processes similar to dendritic cells, such as Langerhans' cells, and interdigitating reticulum cells, present in normal tissues as well as in certain tumors and inflammatory diseases. Manual counting of the S-100 positive cells and fibers revealed both of these to be significantly increased in SIDS infants as compared to age-matched control infants. Morphologically, the bronchiolar dendritic cells closely resembled Langerhans' cells and therefore may have similar immunologic functions, such as antigen presentation and viral and neoantigen immunosurveillance. We hypothesize that the proliferation of these dendritic cells in SIDS victims is a result of exposure to environmental antigens, resulting in a thickening of the bronchiolar walls, narrowing of the lumen, and reduction in airflow, thus causing a chronic or persistent hypoxia.

摘要

婴儿猝死综合征(SIDS)受害者的细支气管壁显著增厚,外膜中的单核细胞增多。对25例SIDS婴儿和18例年龄匹配的对照婴儿进行了免疫组织化学研究,以鉴定这些细胞。抗体组合包括α-1-抗胰蛋白酶、溶菌酶、肌动蛋白、波形蛋白、Leu M1、神经元特异性烯醇化酶(NSE)、S-100、Leu 6、蛙皮素、血清素、抗P物质、血管活性肠肽、MAC 387和因子ⅩⅢa。细支气管细胞用S-100抗体染色,显示出与树突状细胞相似的细长突起,如朗格汉斯细胞和交错突网状细胞,这些细胞存在于正常组织以及某些肿瘤和炎症性疾病中。对S-100阳性细胞和纤维进行人工计数发现,与年龄匹配的对照婴儿相比,SIDS婴儿的这两者均显著增加。从形态学上看,细支气管树突状细胞与朗格汉斯细胞非常相似,因此可能具有相似的免疫功能,如抗原呈递以及病毒和新抗原免疫监视。我们推测,SIDS受害者中这些树突状细胞的增殖是暴露于环境抗原的结果,导致细支气管壁增厚、管腔狭窄和气流减少,从而引起慢性或持续性缺氧。

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