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Blocking interleukin-1 receptors

International Journal of Clinical & Laboratory Research, 1994
During inflammation, injury, immunological challenge or infection, interleukin-1 appears to mediate, in part, the pathogenesis, of disease. Most studies on interleukin-1 are derived from experiments in which bacterial products, such as endotoxins from Gram-negative bacteria or exotoxins from Gram-positive organisms, are used to stimulate macrophagic ...
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Regulation of bovine interleukin-1 receptors

Veterinary Immunology and Immunopathology, 1998
Interleukin-1 is a key player in inflammation and the immune response. The interleukin-1 family consists of three ligands (IL-1 alpha, IL-1 beta, and the IL-1 receptor antagonist) and two receptors (IL-1RI and IL-1RII). Previous studies suggest a dynamic relationship among these receptors and ligands that regulates the magnitude and extent of IL-1 ...
P W, Yu   +8 more
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Interleukin-1 receptor antagonist activity of a human interleukin-1 inhibitor

Nature, 1990
Three interleukin-1 inhibitors have been purified to homogeneity from medium conditioned by human monocytes. Partial sequence analysis and digestion with N-glycanase indicate that these are glycosylation forms of a single protein. The protein binds to the interleukin-1 receptor but has no interleukin-1-like activity, even at very high concentrations ...
C H, Hannum   +9 more
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Expression of interleukin-1 and interleukin-1 receptor antagonists in endometrial cancer

Gynecologic Oncology, 1991
The cytokine interleukin-1 (IL-1) can inhibit growth of breast cancer cells in culture and promote cellular differentiation in synergism with other growth factors. A secreted IL-1 receptor antagonist (sIL-1ra) has been described and an intracellular version (icIL-1ra) has been cloned; both antagonists block IL-1-dependent responses.
L, Van Le   +3 more
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Interleukin-1 Receptor Antagonist

1993
IL-1ra is the first described naturally occurring receptor antagonist of any cytokine or hormone-like molecule. IL-1ra is a member of the IL-1 family by three criteria: amino acid sequence homology of 26 to 30% to IL-1 beta and 19% to IL-1 alpha; similarities in gene structure; and common gene localization to human chromosome 2q14.
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Interleukin‐1 and interleukin‐1 receptor antagonist in inflammatory bowel disease.

Alimentary Pharmacology & Therapeutics, 1996
Ulcerative colitis (UC) and Crohn's disease (CD) are immunologically mediated disorders characterized by a chronic, relapsing inflammatory response. Elevation of several cytokines, with important immunoregulatory and proinflammatory activities have been demonstrated during active inflammatory bowel disease (IBD).
F, Cominelli, T T, Pizarro
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Endogenous Interleukin-1 Receptor Antagonist is Neuroprotective

Biochemical and Biophysical Research Communications, 1997
Interleukin-1 (IL-1) has been implicated in chronic and acute cerebral neuropathologies. IL-1 receptor antagonist (IL-1ra), a naturally occurring protein that binds to IL-1 receptors without inducing signal transduction, blocks several actions of IL-1. IL-1ra acts at the local level and it also circulates in the bloodstream.
Loddick, Sarah A.   +5 more
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Interleukin-1 and Interleukin-1 Receptor Antagonist in Systemic Lupus Erythematosus

Immunological Investigations, 1997
Interleukin-1 (IL-1) is thought to play an important role in the immunopathology of systemic lupus erythematosus (SLE). IL-1 receptor antagonist (IL-1ra) exhibits a dose-responsive inhibition of IL-1 effects, and Fcr receptors play a key role in IL-1ra production.
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Interleukin-1 and interleukin-1 receptor antagonist.

Nutrition (Burbank, Los Angeles County, Calif.), 1996
Cytokines are produced in disease or during immunologic challenge. Some cytokines increase host resistance to disease whereas others trigger inflammatory processes. Interleukin 1 (IL-1) and tumor necrosis factor (TNF) are pro-inflammatory cytokines that affect nearly every cell either alone or in a synergistic fashion.
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The interleukin-1/interleukin-1-receptor interaction

Annales de l'Institut Pasteur / Immunologie, 1987
H R, MacDonald, J W, Lowenthal
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