Beilke M A
Division of Intramural Research, National Institute of Neurological and Communicative Disorders and Stroke, Bethesda, Maryland 20892.
Rev Infect Dis. 1989 Mar-Apr;11(2):273-83. doi: 10.1093/clinids/11.2.273.
During infection the vascular endothelial cell (EC) undergoes important immunologic alterations leading to increased leukocyte-EC adherence and initiation of a host inflammatory response. ECs express class 2 immune response genes and the interleukin 1 gene to a greater degree during infection and thus may be capable of amplifying the lymphocytic proliferative process. Lymphokines generated from stimulated lymphocytes, notably interferon-gamma, may in turn further enhance EC-leukocyte adherence and class 2 antigenic presentation by ECs. The ECs of different organ systems appear variable in terms of their immunologic capabilities. Infection of the endothelium has been demonstrated for an array of human pathogens, and even subclinical infection of ECs may ultimately assume importance in disease processes such as atherosclerosis. A potential role of the EC in the pathogenesis of newer infectious diseases, such as AIDS, is becoming evident and warrants further attention.
在感染过程中，血管内皮细胞（EC）会发生重要的免疫改变，导致白细胞与内皮细胞的黏附增加，并引发宿主炎症反应。内皮细胞在感染期间会更大量地表达2类免疫反应基因和白细胞介素1基因，因此可能有能力放大淋巴细胞增殖过程。受刺激淋巴细胞产生的淋巴因子，尤其是干扰素-γ，反过来可能会进一步增强内皮细胞与白细胞的黏附以及内皮细胞的2类抗原呈递。不同器官系统的内皮细胞在免疫能力方面表现出差异。已证实多种人类病原体可感染内皮，即使是内皮细胞的亚临床感染最终也可能在动脉粥样硬化等疾病过程中发挥重要作用。内皮细胞在诸如艾滋病等新型传染病发病机制中的潜在作用正变得明显，值得进一步关注。
