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Cited by 1,046IL-33, ST2, and ILC PathwaysCytokine Signaling Pathways and InteractionsInflammasome and immune disorders

Interleukin-1 and Related Cytokines in the Regulation of Inflammation and Immunity

Open access
Mantovani, Alberto, Dinarello, Charles A., Molgora, Martina, Garlanda, Cecilia·2019·Immunity
DOI 10.1016/j.immuni.2019.03.012PMC PMC7174020
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Abstract

Forty years after its naming, interleukin-1 (IL-1) is experiencing a renaissance brought on by the growing understanding of its context-dependent roles and advances in the clinic. Recent studies have identified important roles for members of the IL-1 family-IL-18, IL-33, IL-36, IL-37, and IL-38-in inflammation and immunity. Here, we review the complex functions of IL-1 family members in the orchestration of innate and adaptive immune responses and their diversity and plasticity. We discuss the varied roles of IL-1 family members in immune homeostasis and their contribution to pathologies, including autoimmunity and auto-inflammation, dysmetabolism, cardiovascular disorders, and cancer. The trans-disease therapeutic activity of anti-IL-1 strategies argues for immunity and inflammation as a metanarrative of modern medicine.

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Crossref · 10.1016/j.immuni.2019.03.012

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  • The Il1rn gene encodes four isoforms of IL-1R antagonist (IL-1Ra), which regulates inflammatory signaling of the IL-1 pathway by competing with IL-1α and IL-1β in IL-1R activation.

    “The Il1rn gene encodes four isoforms of IL-1R antagonist (IL-1Ra), which regulates the inflammatory signaling of the IL-1 pathway by competing with IL-1α and IL-1β in IL-1R activation”

    From Single-cell transcriptomics unveils skin cell specific antifungal immune responses and IL-1Ra- IL-1R immune evasion strategies of emerging fungal pathogen Candida auris (2024) · cites this paper as [26]

    The section on receptors and negative regulation identifies IL-1Ra as a receptor antagonist that binds IL-1R1; it also says IL-1α and IL-1β use that receptor to signal. This supports the claim about antagonizing their signaling, but our copy does not state that the Il1rn gene encodes four IL-1Ra isoforms. Page numbers were not available in the indexed passages. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • IL-1R signaling is critical for neutrophil function.

    “IL-1R signaling is critical for neutrophil function [26, 31, 32]”

    From Single-cell transcriptomics unveils skin cell specific antifungal immune responses and IL-1Ra- IL-1R immune evasion strategies of emerging fungal pathogen Candida auris (2024) · cites this paper as [26]

    The Hemopoiesis, ageing and innate memory section (page unavailable) says IL-1 promotes neutrophil survival. The Gastrointestinal tract section (page unavailable) also reports IL-1 promoting neutrophil-mediated control of bacterial invasion in a colorectal-cancer study. These support a role for IL-1 signaling in particular neutrophil-related responses, but do not establish that IL-1R signaling is critical for neutrophil function generally. (LLM, conf=0.83)

    Experimental — accuracy not yet measured

  • IL-1Ra is produced predominantly by macrophages in response to C. auris and inhibits IL-1α and IL-1β signaling by competitively binding to IL-1R.

    “IL-1Ra is produced predominantly by macrophages in response to C. auris and inhibits IL-1α and IL-1β signaling by competitively binding to IL-1R [88,89].”

    From Host–Candida auris interactions in the skin (2026) · cites this paper as [88]

    The section on negative regulation identifies IL-1Ra as a receptor antagonist that binds IL-1R1, and the same section says IL-1α and IL-1β signal through that receptor. It does not report that macrophages predominantly produce IL-1Ra in response to C. auris, or explicitly describe its binding as competitive. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

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Cited by

Sorted by citations

Authors
Mantovani, A., Dinarello, C. A., Molgora, M., & Garlanda, C.
Affiliations
  • Humanitas University (IT)
  • Radboud University Medical Center (NL)
  • IRCCS Humanitas Research Hospital (IT)
Corresponding author
Mantovani, Alberto
ORCID
Venue
Immunity
Publisher
Elsevier BV
Published
2019-04
Volume
50
Issue
4
Pages
778-795
ISSN
1074-7613 (ISSN-L)
DOI
10.1016/j.immuni.2019.03.012
PMC
PMC7174020
OpenAlex
W2939625028
Cited by
1,046
References
16
Citations by year
2026: 89 · 2025: 170 · 2024: 174 · 2023: 172 · 2022: 172 · 2021: 140 · 2020: 97 · 2019: 31
FWCI
9.48
Type
journal article
Language
en
Open access
Licence
Locations
  • Immunity (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
  • Radboud Repository (Radboud University) (submittedVersion)
Funders
  • Ministero della Salute (RF-2013-02355470)
  • Ministero dell’Istruzione, dell’Università e della Ricerca (PRIN 2015YYKPNN)
  • Fondazione Cariplo
  • Associazione Italiana per la Ricerca sul Cancro (5x1000 9962, IG 19014, IG 21714, 21147)
  • European Commission (PHII-669415)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › IL-33, ST2, and ILC Pathways
  • Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
Keywords
interleukin-1, IL-1 family cytokines, IL-18, IL-33, IL-36, IL-37, IL-38, innate immunity, adaptive immunity, immune homeostasis, autoimmunity, autoinflammation, metabolic dysfunction, cardiovascular disease, cancer, anti-IL-1 therapy
MeSH terms
Animals, Cardiovascular Diseases, Gastrointestinal Diseases, Multigene Family, Hematopoiesis, Humans, Immunity, Innate, Inflammation, Interleukin-1, Lymphocytes, Neoplasms, Cytokines, Receptors, Cytokine, Mice, Knockout, Neurodegenerative Diseases, Mice, Adaptive Immunity

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