| Interleukin-1 (IL-1) pathway. | |
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MedLine Citation:
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PMID: 20086235 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The interleukin-1 (IL-1) family of cytokines comprises 11 proteins (IL-1F1 to IL-1F11) encoded by 11 distinct genes in humans and mice. IL-1-type cytokines are major mediators of innate immune reactions, and blockade of the founding members IL-1alpha or IL-1beta by the interleukin-1 receptor antagonist (IL-1RA) has demonstrated a central role of IL-1 in a number of human autoinflammatory diseases. IL-1alpha or IL-1beta rapidly increase messenger RNA expression of hundreds of genes in multiple different cell types. The potent proinflammatory activities of IL-1alpha and IL-1beta are restricted at three major levels: (i) synthesis and release, (ii) membrane receptors, and (iii) intracellular signal transduction. This pathway summarizes extracellular and intracellular signaling of IL-1alpha or IL-1beta, including positive- and negative-feedback mechanisms that amplify or terminate the IL-1 response. In response to ligand binding of the receptor, a complex sequence of combinatorial phosphorylation and ubiquitination events results in activation of nuclear factor kappaB signaling and the JNK and p38 mitogen-activated protein kinase pathways, which, cooperatively, induce the expression of canonical IL-1 target genes (such as IL-6, IL-8, MCP-1, COX-2, IkappaBalpha, IL-1alpha, IL-1beta, MKP-1) by transcriptional and posttranscriptional mechanisms. Of note, most intracellular components that participate in the cellular response to IL-1 also mediate responses to other cytokines (IL-18 and IL-33), Toll-like-receptors (TLRs), and many forms of cytotoxic stresses. |
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Authors:
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Axel Weber; Peter Wasiliew; Michael Kracht |
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Publication Detail:
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Type: Journal Article; Review Date: 2010-01-19 |
Journal Detail:
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Title: Science signaling Volume: 3 ISSN: 1937-9145 ISO Abbreviation: Sci Signal Publication Date: 2010 |
Date Detail:
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Created Date: 2010-01-20 Completed Date: 2010-05-13 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 101465400 Medline TA: Sci Signal Country: United States |
Other Details:
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Languages: eng Pagination: cm1 Citation Subset: IM |
Affiliation:
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Rudolf-Buchheim-Institute of Pharmacology, Justus-Liebig-University Giessen, 35392 Giessen, Germany. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Cytokines / metabolism Feedback, Physiological Humans Interleukin-1 / metabolism* Signal Transduction* |
| Chemical | |
Reg. No./Substance:
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0/Cytokines; 0/Interleukin-1 |
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