Vascular endothelium in immunology and infectious disease.
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.
Beilke
M A
MA
Division of Intramural Research, National Institute of Neurological and Communicative Disorders and Stroke, Bethesda, Maryland 20892.
D000163:Acquired Immunodeficiency Syndrome / Q000276:immunology / Q000382:microbiology / Q000473:pathology; D002448:Cell Adhesion; D002478:Cells, Cultured; D004730:Endothelium, Vascular / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D006678:HIV / Q000502:physiology; D000949:Histocompatibility Antigens Class II / Q000096:biosynthesis; D006801:Humans; D007239:Infections / Q000276:immunology* / Q000473:pathology; D007962:Leukocytes / Q000473:pathology; D018406:Virus Physiological Phenomena
D000949:Histocompatibility Antigens Class II