Immunological and inflammatory functions of the interleukin-1 family
Abstract
More than any other cytokine family, the interleukin (IL)-1 family is closely linked to the innate immune response. This linkage became evident upon the discovery that the cytoplasmic domain of the IL-1 receptor type I is highly homologous to the cytoplasmic domains of all Toll-like receptors (TLRs). Thus, fundamental inflammatory responses such as the induction of cyclooxygenase type 2, increased expression of adhesion molecules, or synthesis of nitric oxide are indistinguishable responses of both IL-1 and TLR ligands. Both families nonspecifically affect antigen recognition and lymphocyte function. IL-1beta is the most studied member of the IL-1 family because of its role in mediating autoinflammatory diseases. Although the TLR and IL-1 families evolved to assist in host defense against infection, unlike the TLR family, the IL-1 family also includes members that suppress inflammation, both specifically within the IL-1 family but also nonspecifically for TLR ligands and the innate immune response.
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IL-1β is known to induce a proinflammatory Mp phenotype.
“Since IL-1β, in turn, is known to induce a proinflammatory Mp phenotype (15,21)”
From Sustained Inflammasome Activity in Macrophages Impairs Wound Healing in Type 2 Diabetic Humans and Mice (2014) · cites this paper as [21]
The NLRP-3 inflammasome plays a role in the pathophysiology of many inflammatory diseases, including obesity, insulin resistance, and diabetes.
“The NLRP-3 inflammasome plays a role in the pathophysiology of many inflammatory diseases, including obesity, insulin resistance, and diabetes (21,31–35).”
From Sustained Inflammasome Activity in Macrophages Impairs Wound Healing in Type 2 Diabetic Humans and Mice (2014) · cites this paper as [21]
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IL-1H, AN INTERLEUKIN 1-RELATED PROTEIN THAT BINDS IL-18 RECEPTOR/IL-1Rrp
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Interleukin-1 induces interleukin-8 secretion from endothelial cells by a juxtacrine mechanism
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Self-citationMEFV mutation analysis in patients suffering from amyloidosis of familial Mediterranean fever
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Self-citationIL-12–induced IFN-γ is dependent on caspase-1 processing of the IL-18 precursor
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Self-citationIdentification and Gene Organization of Three Novel Members of the IL-1 Family on Human Chromosome 2
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IL-1 Receptor Accessory Protein Is an Essential Component of the IL-1 Receptor
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Interleukin-18 controls energy homeostasis by suppressing appetite and feed efficiency
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A Novel Therapy of Murine Collagen-Induced Arthritis with Soluble T1/ST2
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Interleukin‐1β, but not interleukin‐1α, is required for T‐cell‐dependent antibody production
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Mechanisms of Inhibition of Collagen-Induced Arthritis by Murine IL-18 Binding Protein
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HMG-1 REDISCOVERED AS A CYTOKINE
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Resistant Behçet Disease Responsive to Anakinra
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Self-citationInterleukin-1 receptor antagonist in normal and psoriatic epidermis.
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The N-terminal propiece of interleukin 1α is a transforming nuclear oncoprotein
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Self-citationThe many worlds of reducing interleukin‐1
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IL1HY1: A Novel Interleukin-1 Receptor Antagonist Gene
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Self-citationThe Membrane Form of the Type II IL-1 Receptor Accounts for Inhibitory Function
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Self-citationIdentification of Amino Acid Residues Critical for Biological Activity in Human Interleukin-18
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Self-citationIL-33: A Sheep in Wolf’s Clothing?
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Antiviral and immunoregulatory activities of IFN-γ depend on constitutively expressed IL-1α
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Protective Effect of IL-18 on Kainate- and IL-1β-Induced Cerebellar Ataxia in Mice
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EVIDENCE THAT HAX-1 IS AN INTERLEUKIN-1α N-TERMINAL BINDING PROTEIN
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Self-citationCharacterization of Binding Properties of ICAM‐1 Peptides to LFA‐1: Inhibitors of T‐cell Adhesion
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NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals
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- Authors
- Dinarello, C. A.
- Affiliations
- University of Colorado Anschutz (US)
- Corresponding author
- Dinarello, Charles A.
- Venue
- Annual Review of Immunology
- Publisher
- Annual Reviews
- Published
- 2009-04-01
- Volume
- 27
- Issue
- 1
- Pages
- 519-550
- ISSN
- 0732-0582 (ISSN-L)
- 1545-3278
- OpenAlex
- W2165275387
- Cited by
- 3,466
- References
- 170
- Citations by year
- 2026: 95 · 2025: 169 · 2024: 195 · 2023: 185 · 2022: 209 · 2021: 183 · 2020: 199 · 2019: 202 · 2018: 231 · 2017: 219 · 2016: 198 · 2015: 223 · 2014: 244 · 2013: 227 · 2012: 206
- FWCI
- 17.82
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Annual Review of Immunology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Allergy and Infectious Diseases (AI‑15614)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Keywords
- interleukin-1 family, innate immunity, inflammation, Toll-like receptors, IL-1 receptor type I, IL-1β, autoinflammatory disease, adhesion molecules, nitric oxide, antigen recognition, lymphocyte function, anti-inflammatory cytokines
- MeSH terms
- NLR Family, Pyrin Domain-Containing 3 Protein, Animals, B-Lymphocytes, Carrier Proteins, T-Lymphocytes, Helper-Inducer, Humans, Immunity, Innate, Inflammation, Interleukin-1, Signal Transduction, Receptors, Interleukin-1, Receptors, Purinergic P2, Caspase 1, Toll-Like Receptors, Receptors, Purinergic P2X7
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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