Both immunological and inflammatory reactions are mediated by a group of hormone-like polypeptides referred to as interleukins. Interleukins are secreted by cells that make up the immune system, such as lymphocytes and macrophages, and may be secreted by other non-immunological cells types as well, including epidermal cells and polymorphonuclear leukocytes. Interleukin-like molecules have been studied by immunologists and cell biologists for many years and were described primarily by their biological effects, ie., T and B cell growth factors, mitogenic factors, endogenous pyrogen, and ymphocyte activating factors. In the late 1970s an informal convention for nomenclature was agreed upon whereby molecules related to while blood cell function were termed inter-leukins (IL). There are currently four such designated molecules, IL-1, IL-2, IL-3, and IL-4. Interleukin-1, formerly known as lymphocyte activating factor (LAF) or endogenous pyrogen, is a 17 kDa glycoprotein produced primarily by mactophages that exerts a number of immunostimulatory and pro-inflammatory effects. Interleukin-2, formerly known as T cell growth factor or mitogenic factor, is a 15 kDa polypeptide that induces growth and division in T and B lymphocytes and activates natural killer (NK) cells. Interleukin-3 is a 25 kDa polypeptide that acts as a differentiating factor for numerous hemopoietic stem cells and mast cells, and is also known as panspecific hemopoietin (PSH). Interleukin-4 refers to activities previously termed B cell growth factor and eosinophil differentiating factor, and is a 44 kDa polypeptide. More recent work from our laboratory as well as several other laboratories suggests that there exists a family of molecules that regulate the effects of some of the interleukins. The best studied of these include three molecules that appear to be specific inhibitors of interleukin-1. These include a 30-35 kDa glycoprotein termed febrile inhibitor derived from the urine of febrile individuals, an 85 kDa glycoprotein termed uromodulin derived from the urine of pregnant women, and a 20-25 kDa molecule derived either from the urine of patients with myelomonocytic leukemia, or from the supernatants of cultured and stimulated macrophages. Both the febrile inhibitor and uromodulin block interleukin-1 induced T cell differentiation, but augment interleukin-1 induced prostaglandin production by fibroblasts. The 20-25 kDa inhibitor inhibits both T cell differentiation as well as the effects of IL-1 on fibroblasts. Although studies on these interleukin-1 inhibitors are in their relative scientific infancy, they suggest that these molecules may be part of a family of physiological regulators of interleukin-1.
|Original language||English (US)|
|Number of pages||9|
|Journal||Einstein Quarterly Journal of Biology and Medicine|
|Publication status||Published - Jan 1 1987|
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