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Cited by 1,866Immune Response and InflammationInflammasome and immune disordersIL-33, ST2, and ILC Pathways

Overview of the IL ‐1 family in innate inflammation and acquired immunity

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Dinarello, Charles A.·2018·Immunological Reviews
DOI 10.1111/imr.12621PMC PMC5756628
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Abstract

Summary: The interleukin‐1 (IL‐1) family of cytokines and receptors is unique in immunology because the IL‐1 family and Toll‐like receptor (TLR) families share similar functions. More than any other cytokine family, the IL‐1 family is primarily associated with innate immunity. More than 95% of living organisms use innate immune mechanisms for survival whereas less than 5% depend on T‐ and B‐cell functions. Innate immunity is manifested by inflammation, which can function as a mechanism of host defense but when uncontrolled is detrimental to survival. Each member of the IL‐1 receptor and TLR family contains the cytoplasmic Toll‐IL‐1‐Receptor (TIR) domain. The 50 amino acid TIR domains are highly homologous with the Toll protein in Drosophila . The TIR domain is nearly the same and present in each TLR and each IL‐1 receptor family. Whereas IL‐1 family cytokine members trigger innate inflammation via IL‐1 family of receptors, TLRs trigger inflammation via bacteria, microbial products, viruses, nucleic acids, and damage‐associated molecular patterns (DAMPs). In fact, IL‐1 family member IL‐1a and IL‐33 also function as DAMPs. Although the inflammatory properties of the IL‐1 family dominate in innate immunity, IL‐1 family member can play a role in acquired immunity. This overview is a condensed update of the IL‐1 family of cytokines and receptors.

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  • IL-1 activates numerous signaling pathways that directly impact protein synthesis and cell cycle activity, including PI3K/Akt, p38 MAPK, MEK/ERK, and RAS.

    “IL-1 activates numerous signaling pathways that directly impact protein synthesis and cell cycle activity, including PI3K/Akt, p38 MAPK, MAPK/ERK kinase (MEK)/ERK, and RAS (Dinarello, 2018).”

    From PU.1 enforces quiescence and limits hematopoietic stem cell expansion during inflammatory stress (2021) · cites this paper as Dinarello, 2018

    Section 2.2 (page unavailable) says IL-1 binding triggers a kinase cascade that activates NFκB, supporting the general point that IL-1 initiates signaling. It does not identify PI3K/Akt, p38 MAPK, MEK/ERK, or RAS as pathways activated by IL-1, or link those pathways to protein synthesis and cell-cycle activity; searches for those terms found no supporting passage. (LLM, conf=0.85)

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Authors
Dinarello, C. A.
Affiliations
Radboud University Medical Center (NL)
Corresponding author
Dinarello, Charles A.
ORCID
Dinarello, Charles A.
Venue
Immunological Reviews
Publisher
Wiley
Published
2017-12-16
Volume
281
Issue
1
Pages
8-27
ISSN
  • 0105-2896 (ISSN-L)
  • 1600-065X
DOI
10.1111/imr.12621
PMC
PMC5756628
OpenAlex
W2771968994
Cited by
1,866
References
10
Citations by year
2026: 225 · 2025: 266 · 2024: 284 · 2023: 246 · 2022: 270 · 2021: 239 · 2020: 205 · 2019: 92 · 2018: 37 · 2017: 1
FWCI
9.41
Type
journal article
Language
en
Open access
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations
  • Immunological Reviews (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
  • Radboud Repository (Radboud University) (submittedVersion)
Funders
National Institutes of Health (AI15614)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
  • Life Sciences › Immunology and Microbiology › Immunology › IL-33, ST2, and ILC Pathways
Keywords
interleukin-1 family, IL-1 receptor, Toll-like receptors, TIR domain, innate immunity, inflammation, damage-associated molecular patterns, interleukin-1 alpha, IL-33, adaptive immunity, host defense
MeSH terms
Interleukin-33, Animals, Drosophila, Humans, Immunity, Innate, Inflammation, Interleukin-1, Receptors, Interleukin-1, Toll-Like Receptors, Adaptive Immunity

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