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Abstract

Many pathways have led to the discovery of interleukin-1 (IL-1) as a distinct molecule. In the 1940s Menkin (1945) suggested that fever was caus ed by a soluble factor released by activated perito neal exudate cells. The substance was called pyrexin and later granulocytic pyrogen. Subsequently a cir culating pyrogen called endogenous pyrogen was demonstrated in rabbits. After some years a macrophage product, leukocyte endogenous medi ator, was found to induce the acute phase response. In 1972 an apparently unrelated biological re sponse, augmentation of thymocyte proliferation, was ascribed to the lymphocyte activating factor (Gery et al. 1972). At that time there was increasing confusion about the terminology as all the afore mentioned activities were supposed to be caused by the same molecule, or a family of closely related molecules. This led to an agreement in 1979 that all the factors described above should be termed IL-1 (Aarden et al. 1979). An importent step forward in the history of IL-1 was the cloning and expression of the gene encoding human IL-1, which was achieved by several groups in 1984–1985. It was found that two different genes were capable of ex pressing IL-1 activities, and the proteins were termed IL-1α and IL-1 β.

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Waage, A., Redl, H., Schlag, G., Schade, U. (1993). The Cytokine Network in Sepsis II: IL-1 and IL-6. In: Schlag, G., Redl, H. (eds) Pathophysiology of Shock, Sepsis, and Organ Failure. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-76736-4_36

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