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- W1971295881 endingPage "S66" @default.
- W1971295881 startingPage "S62" @default.
- W1971295881 abstract "Since the discovery that epidermal cell-derived thymocyte-activating factor was identical to interleukin (IL)-1 alpha and -beta in 1986, these molecules have been implicated in the pathogenesis of skin diseases. In 1995, it has become clear that a group of gene products function to regulate the activity of IL-1. IL-1 alpha and mature 17-kD IL-1 beta (cleaved from precursor by IL-1 beta-converting enzyme) bind to the type 1 IL-1 receptor to transduce a signal. This process can be antagonized at the level of the receptor by two distinct forms of the IL-1 receptor antagonist, which bind to the type I receptor but do not transduce a signal. The process can also be antagonized at the level of the ligand by either cell-bound or soluble type 2 IL-1 receptor. This type 2 IL-1 receptor binds ligand but does not transduce a signal. Keratinocytes can make each of these variables in vitro, and the balance between agonists and antagonists dictates the biologic outcome of a putative IL-1-mediated event. Transgenic mice that overexpress each of these factors individually in epidermis will be useful for enhancing our understanding of the cutaneous biology of IL-1." @default.
- W1971295881 created "2016-06-24" @default.
- W1971295881 creator A5083529701 @default.
- W1971295881 creator A5091128223 @default.
- W1971295881 date "1995-07-01" @default.
- W1971295881 modified "2023-10-16" @default.
- W1971295881 title "The Interleukin-1 Axis and Cutaneous Inflammation" @default.
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