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The interleukin‐1 family: 10 years of discovery 1
Abstract
Ten years ago the cloning of two interleukin-1 molecules (IL-1 alpha and IL-1 beta) resolved the question of whether a single polypeptide could evoke a wide variety of biological effects. During the past decade, the biology of IL-1 has greatly expanded our understanding of how the host responds to external challenges, such as injury and infection, as well as its role in several diseases. We learned of the remarkable potency of IL-1 in the femtomolar range and of its ability to induce a response by triggering only one or two receptors per cell. Unexpectedly, the IL-1 family of genes, receptors and associated molecules have been linked to those of Drosophila, nematodes, and microorganisms and IL-1 signal transduction is similar to that observed after cellular stress. The cloning of IL-1 opened other avenues of fundamental biological interest. For example, in addition to the two agonist molecules IL-1 alpha and IL-1 beta, a third member of the IL-1 gene family is a specific, high affinity receptor antagonist (IL-1 receptor antagonist). That this third member of the IL-1 family inhibits the other two is characteristic of the tight control over production and activity exerted on IL-1. Although IL-1 contributes to the pathogenesis of many diseases, a small amount appears to be needed to combat infection and initiate healing processes. This article highlights 10 years of discoveries on IL-1.
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In the citing paper
“IL‐1ra inhibits IL‐1β signal transduction (211) and IL‐10 inhibits synthesis of TNF‐α (212).”
From Muscle–Organ Crosstalk: The Emerging Roles of Myokines (2020) · cites this paper as [211]
In the citing paper
“IL-1RA inhibits IL-1β signal transduction126”
From Exerkines in health, resilience and disease (2022) · cites this paper as [126]
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“Such cross-regulation is not unique to IL-6 and TNF-a since, for example, IL-1 can also induce IL-6 production (Legrand-Poels et al., 2000) and have an indirect impact on immune cell recruitment (Dinarello, 1994).”
Background
Metadata
- Authors
- Dinarello, C. A.
- Affiliations
- Tufts University (US)
- Corresponding author
- Dinarello, Charles A.
- Venue
- The FASEB Journal
- Publisher
- Wiley
- Published
- 1994-12
- Volume
- 8
- Issue
- 15
- Pages
- 1314-1325
- ISSN
- 0892-6638 (ISSN-L)
- 1530-6860
- OpenAlex
- W1514081838
- Cited by
- 783
- References
- 0
- Citations by year
- 2025: 8 · 2024: 8 · 2023: 8 · 2022: 14 · 2021: 17 · 2020: 21 · 2019: 14 · 2018: 11 · 2017: 19 · 2016: 17 · 2015: 23 · 2014: 27 · 2013: 23 · 2012: 26
- FWCI
- 18.09
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The FASEB Journal (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Allergy and Infectious Diseases (AI‑15614)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Cytokine Signaling Pathways and Interactions
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Keywords
- interleukin-1, IL-1α, IL-1β, interleukin-1 receptor antagonist, IL-1 receptor, Drosophila, nematodes, microorganisms, host response to infection, host response to injury, pathogenesis, cytokine regulation
- MeSH terms
- Animals, Humans, Interleukin-1, Structure-Activity Relationship, Signal Transduction, Receptors, Interleukin-1
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