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Cited by 1,532

The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.

Biology of interleukin 1

Dinarello, Charles A.·1988·The FASEB Journal

Abstract

Interleukin 1 (IL 1) is a polypeptide that is produced after infection, injury, or antigenic challenge. Although the macrophage is a primary source of IL 1, epidermal, epithelial, lymphoid, and vascular tissues synthesize IL 1. When IL 1 gains access to the circulation, it acts like a hormone and induces a broad spectrum of systemic changes in neurological, metabolic, hematologic, and endocrinologic systems. Some of the IL 1 that is synthesized remains associated with the plasma membrane and induces changes in local tissues without producing systemic responses. IL 1 affects mesenchymal tissue remodeling where it contributes to both destructive and repair processes. IL 1 activates lymphocytes and plays an important role in the initiation of the immune response. Receptors for IL 1 have been identified, but receptors are scarce and their affinities often do not match the potency of the biological response. The most consistent property of IL 1 is up‐regulation of cellular metabolism and increased expression of several genes coding for biologically active molecules. IL 1 is a highly inflammatory molecule and stimulates the production of arachidonic acid metabolites. IL 1 also acts synergistically with other cytokines, particularly tumor necrosis factor. The multitude of biological responses to IL 1 is an example of the rapid adaptive changes that take place to increase the host's defensive mechanisms.—D inarello , C. A. Biology of interleukin 1. FASEB J. 2: 108‐115; 1988.

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Metadata

Authors
Dinarello, C. A.
Venue
The FASEB Journal
Publisher
Wiley
Published
1988-02
Volume
2
Issue
2
Pages
108-115
ISSN
  • 0892-6638 (ISSN-L)
  • 1530-6860
OpenAlex
W1848552725
Cited by
1,532
References
1
FWCI
83.42
Type
journal article
Language
en
Open access
closed

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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