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炎症
Vol. 9 (1988-1989) No. 4 P 303-308

記事言語:

http://doi.org/10.2492/jsir1981.9.303


On inflammatory initiation, macrophages are enhanced in their capacity to produce reactive oxygen intermediates such as O-2 and H2O2, and kill microbes for host survival from infection. Contrary to the initiation, the mechanism to cease inflammation is hardly understood. Since permanent producing of reactive oxygen intermediates is toxic, the host itself probably requires the ability to deactivate macrophages. Macrophages are essential to the healing of wounds and repair of tissue damaged by inflammation. These concepts led us to search for macrophage deactivating effects among polypeptide growth factors that regulate angiogenesis, fibrogenesis and other aspects of tissue repair. Among 12 such factors, two polypeptides that possess 71% similar homology proved to be potent macrophage deactivators: transforming growth factor-β1 (TGF-β1) and TGF-β2.
The fact that their concentrations for 50% inhibition were extremely low of picomolar level, suggests TGF-β play a powerful role on ceasing the inflammation and tissue repair after an inflammation site has been sterilized. Although the deactivating site by TGF-β existed in anabolism but nct catabolism of reactive oxygen intermediates, exact site is not yet determined.

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