Interleukin 1α and the inflammatory process
Open accessAbstract
Inflammation occurs after disruption of tissue homeostasis by cell stress, injury or infection and ultimately involves the recruitment and retention of cells of hematopoietic origin, which arrive at the affected sites to resolve damage and initiate repair. Interleukin 1α (IL-1α) and IL-1β are equally potent inflammatory cytokines that activate the inflammatory process, and their deregulated signaling causes devastating diseases manifested by severe acute or chronic inflammation. Although much attention has been given to understanding the biogenesis of IL-1β, the biogenesis of IL-1α and its distinctive role in the inflammatory process remain poorly defined. In this review we examine key aspects of IL-1α biology and regulation and discuss its emerging importance in the initiation and maintenance of inflammation that underlie the pathology of many human diseases.
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Both IL-1α and IL-1β cytokines are expressed as precursor proteins; pro-IL-1β requires proteolytic cleavage to be bioactive, while such processing is not essential for pro-IL-1α.
“Both IL-1α and IL-1β cytokines are expressed as precursor proteins. While pro-IL-1β requires proteolytic cleavage to be bioactive, such processing is not essential for pro-IL-1α.53”
From TLR9-independent CD8+ T cell responses in hepatic AAV gene transfer through IL-1R1-MyD88 signaling (2024) · cites this paper as [53]
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References 109 · Cited by 568
- Authors
- Di Paolo, N. C., & Shayakhmetov, D. M.
- Affiliations
- Emory University (US)
- Corresponding author
- Shayakhmetov, Dmitry M
- Venue
- Nature Immunology
- Published
- 2016-07-19
- Volume
- 17
- Issue
- 8
- Pages
- 906-913
- ISSN
- 1529-2908 (ISSN-L)
- 1529-2916
- PMC
- PMC5152572
- OpenAlex
- W2498839525
- Cited by
- 568
- References
- 109
- Citations by year
- 2026: 44 · 2025: 57 · 2024: 59 · 2023: 63 · 2022: 76 · 2021: 72 · 2020: 69 · 2019: 46 · 2018: 38 · 2017: 36 · 2016: 8
- FWCI
- 3.86
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Immunology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Allergy and Infectious Diseases (R01AI123126, R21AI126816, R01AI065429, R01AI107960)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Keywords
- interleukin-1 alpha, IL-1β, inflammation, inflammatory cytokines, tissue homeostasis, acute and chronic inflammation, inflammatory disease pathogenesis
- MeSH terms
- Alarmins, Animals, Cell Membrane, Gene Expression Regulation, Granuloma, Humans, Inflammation, Macrophages, Mice, Inbred BALB C, Models, Biological, Neoplasms, Protein Binding, Protein Processing, Post-Translational, Protein Biosynthesis, Signal Transduction, Receptors, Interleukin-1, Mice, Interleukin-1alpha
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