Cell adhesion molecules and cutaneous inflammation.
Cutaneous inflammation is characterized by the infiltration of leukocytes such as polymorphonuclear neutrophils (PMNs), lymphocytes, and monocytes into the epidermis, dermis, or subcutaneous tissue in response to infectious or immunologic stimuli, in wound healing, or in response to trauma. In recent years, it has been found that cell-surface proteins on leukocytes, endothelial cells, and keratinocytes are critical elements in the initiation and evolution of cutaneous inflammation. In order for peripheral blood leukocytes to leave the circulatory system and enter tissue parenchyma, they must first bind to endothelial cells, pass between them, and traverse the vascular basement membrane. In this article we will examine both leukocyte-endothelial cell binding and evidence indicating that various cell-surface molecules present on leukocytes and endothelial cells, known as cell adhesion molecules (CAMs), interact with one another in specific fashion. This interaction or binding is a critical occurrence and its inhibition leads to downregulation of inflammation. Furthermore, some CAMs can be either induced or upregulated on leukocytes and endothelial cells by various proinflammatory cytokines. This tends to upregulate inflammation. It has become increasingly clear that the time-course of inflammation and its exquisite anatomic specificity are related to the regulation of expression of CAMs.
Department of Dermatology, Emory University School of Medicine, Atlanta, GA 30322.
T J
TJ
Lawley
Y
Y
Kubota
D000818:Animals; D015815:Cell Adhesion Molecules / Q000378:metabolism / Q000502:physiology*; D003872:Dermatitis / Q000503:physiopathology*; D015536:Down-Regulation; D004727:Endothelium / Q000378:metabolism; D006801:Humans; D015603:Keratinocytes / Q000378:metabolism; D012867:Skin / Q000378:metabolism
D015815:Cell Adhesion Molecules