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Interleukin 1 and tumour necrosis factor stimulate endothelial cell activation, altering cell surface molecules and vascular function to participate in the inflammatory response.
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The endothelium is now recognised as not simply being an inert lining to blood vessels, as thought in the 1960s, but a highly specialised, metabolically active interface between blood and the underlying tissues—maintaining vascular tone, thromboresistance, and a selective permeability to cells and proteins. Moreover, under the stimulation of agents such as interleukin 1, the endothelium undergoes changes which allow it to participate in the inflammatory response; this is known as endothelial cell activation. The term was coined in the 1960s by Willms-Kretschmer.1 He noted that in delayed hypersensitivity reactions the endothelium became plump and leaky and displayed increased quantities of biosynthetic organelles such as endoplasmic reticulum.1 He used the term activated to imply a change in function as well as morphology. In the 1980s an avalanche of papers showed that the newly discovered cytokines, interleukin 1 and tumour necrosis factor, changed surface molecules and thus the functions of cultured endothelial cells. To emphasise that these changes did not represent injury or dysfunction, Pober reintroduced the term …
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Hunt et al. (1998) conducted a review in Endothelial cell activation and inflammatory response. Cytokines (interleukin 1 and tumour necrosis factor) was evaluated. Interleukin 1 and tumour necrosis factor stimulate endothelial cell activation, altering cell surface molecules and vascular function to participate in the inflammatory response.
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