IL-1


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Related to IL-1: Il-6, IL-2, Cytokines, IL-8, Interleukin 1, IL-1 beta

IL-1

abbreviation for interleukin-1.

IL1B

A gene on chromosome 2q14 that encodes interleukin-1B, a cytokine produced by activated macrophages as a proprotein, which is proteolytically activated by caspase 1 (CASP1/ICE). IL-1B is a key mediator of inflammation and is involved in an array of cellular activities, including cell proliferation, differentiation and apoptosis.

IL-1

Leukocyte-activating factor An 11 kD cytokine produced by a wide range of cells; IL-1 elicits the acute phase response, acts on the CNS as a pyrogen, stimulates fibroblast, B- and T-cell proliferation and differentiation, ↑ lymphokine, collagenase and PG production, activity of NK cells against tumor targets, stimulates myocytolysis–via PGs, elicits hormone release from the pituitary, evokes the release of PMNs from the BM, and PMN degranulation, ↑ oxidase activity and hexose monophosphate shunt activity; in synovial cells, IL-1 stimulates proliferation and production of collagen, PG, and plasminogen activator IL-1 production Stimulated by various agents–eg, calcium ionophores, IFN-α, IFN-γ, lipopolysaccharides, muramyl dipeptide, aluminum hydroxide, phorbol myristate acetate, staphylococci, silica, and others; inhibited by corticosteroids, PGE2–via the cyclooxygenase pathway, suppressor T cells, and cyclosporine–which specifically inhibits T cell-induced IL-1 production IL-1 & disease IL-1 may have a role in
1. Type 1 DM, ↑ IL-1
production by macrophages in the early β-cell destructive lesions of type 1 DM.
2. ASHD–n-3 fish oils ↓ circulating IL-1.
3. Rheumatoid arthritis–IL-1 acts with substance P.

IL-1

α Therapeutic uses IL-1α is reportedly effective in accelerating recovery of platelet counts after high-dose carboplatin and may be useful in thrombocytopenia induced by chemotherapy

IL-1

References in periodicals archive ?
Single nucleotide polymorphisms in intron 2 of the human interleukin-1 receptor antagonist (IL-1Ra) gene: further definition of the IL-1 R and IL-1Ra polymorphisms in North American Caucasians and Taiwanese Chinese.
Allelic frequencies of IL-1 polymorphisms in several ethnic populations.
All pre-specified secondary and exploratory endpoints in both studies demonstrated statistically significant effects of the IL-1 Trap compared to placebo.
An exploratory "responder" analysis of Part A indicated that 70% of patients treated with the IL-1 Trap had at least a 75% reduction in their symptom score compared with 0% of patients treated with placebo (p<0.
Stanford's Robert Sapolsky and his colleagues report that IL-1 did not cause ACTH secretion.
In many cases IL-1 acts as a messenger to help regulate immune and inflammatory responses by attaching to cell-surface receptors in cells that participate in the body's immune system.
In addition, at the American Heart Association Scientific Sessions meeting in November 2005, the Company will report positive preliminary data from a pilot study indicating that the IL-1 Trap provided prolonged suppression of C-reactive Protein (CRP), a marker of inflammation, in otherwise healthy adults.
Certain statements contained herein are "forward-looking" statements including statements regarding our ability to develop diagnostic, personalized nutritional and therapeutic products to prevent or treat diseases of inflammation, our ability to screen nutritional compounds for their effects on inflammatory responses, given specific IL-1 genetic patterns and our ability to make progress in advancing our core technologies.
After evaluating the results of the Phase II study, Novartis informed Regeneron that as a condition for participating in the continued clinical development of the IL-1 Trap, it would require revisions to the terms of the original agreement applicable to the IL-1 Trap.
Since the IL-1 SNPs that an individual is born with do not change, they may be used to predict risk for osteoporosis at any age and to guide development and aid individuals' selection of preventive therapies prior to the development of symptoms.
Studies conducted by Interleukin Genetics have demonstrated that certain variations (SNPs) in the IL-1 genes produce lifelong tendencies to have more inflammation or qualitative differences in inflammation mechanisms.