The DOI matches its Crossref record; 228 of the 228 references it cites were found in a registry or an index.
Inflammasome-Independent Regulation of IL-1-Family Cytokines
Open accessAbstract
Induction, production, and release of proinflammatory cytokines are essential steps to establish an effective host defense. Cytokines of the interleukin-1 (IL-1) family induce inflammation and regulate T lymphocyte responses while also displaying homeostatic and metabolic activities. With the exception of the IL-1 receptor antagonist, all IL-1 family cytokines lack a signal peptide and require proteolytic processing into an active molecule. One such unique protease is caspase-1, which is activated by protein platforms called the inflammasomes. However, increasing evidence suggests that inflammasomes and caspase-1 are not the only mechanism for processing IL-1 cytokines. IL-1 cytokines are often released as precursors and require extracellular processing for activity. Here we review the inflammasome-independent enzymatic processes that are able to activate IL-1 cytokines, paying special attention to neutrophil-derived serine proteases, which subsequently induce inflammation and modulate host defense. The inflammasome-independent processing of IL-1 cytokines has important consequences for understanding inflammatory diseases, and it impacts the design of IL-1-based modulatory therapies.
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“the literature suggests that IL-1β can also be processed to a mature cytokine through inflammasome-independent pathways.54”
From TLR9-independent CD8+ T cell responses in hepatic AAV gene transfer through IL-1R1-MyD88 signaling (2024) · cites this paper as [54]
In the citing paper
“several inflammasome-independent or noncanonical pathways have been characterized, which also result in caspase activation and maturation of IL-1β (Netea et al, 2015).”
From Danger Signals and Inflammasomes: Stress-Evoked Sterile Inflammation in Mood Disorders (2017) · cites this paper as Netea et al, 2015
In the citing paper
“inflammasome-dependent activation of IL-1β is cell type specific (Netea et al, 2015).”
From Danger Signals and Inflammasomes: Stress-Evoked Sterile Inflammation in Mood Disorders (2017) · cites this paper as Netea et al, 2015
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Cites
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Cited by
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Microglial M1/M2 polarization and metabolic states
Orihuela, R., McPherson, C. A., & Harry, G. J. (2016) · British Journal of Pharmacology · doi:10.1111/bph.13139 · Cited by 2,070
Cytokines in Inflammatory Disease
Kany, S., Vollrath, J. T., & Relja, B. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20236008 · Cited by 1,761
Identification of a selective and direct NLRP3 inhibitor to treat inflammatory disorders
Jiang, H., He, H., Chen, Y., Huang, W., Cheng, J., Ye, J., Wang, A., Tao, J., Wang, C., Liu, Q., et al. (2017) · The Journal of Experimental Medicine · doi:10.1084/jem.20171419 · Cited by 783
Limiting inflammation—the negative regulation of NF-κB and the NLRP3 inflammasome
Afonina, I. S., Zhong, Z., Karin, M., & Beyaert, R. (2017) · Nature Immunology · doi:10.1038/ni.3772 · Cited by 785
Immune defence against Candida fungal infections
Netea, M. G., Joosten, L. A. B., van der Meer, J. W. M., Kullberg, B.-J., & van de Veerdonk, F. L. (2015) · Nature Reviews Immunology · doi:10.1038/nri3897 · Cited by 642
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Metadata
- Authors
- Netea, M. G., van de Veerdonk, F. L., van der Meer, J. W. M., Dinarello, C. A., & Joosten, L. A. B.
- Affiliations
- Radboud University Medical Center (NL)
- Department of Internal Medicine,
- University of Colorado Anschutz (US)
- Venue
- Annual Review of Immunology
- Publisher
- Annual Reviews
- Published
- 2015-03-21
- Volume
- 33
- Issue
- 1
- Pages
- 49-77
- ISSN
- 0732-0582 (ISSN-L)
- 1545-3278
- OpenAlex
- W2156301166
- Cited by
- 326
- References
- 228
- Citations by year
- 2026: 8 · 2025: 6 · 2024: 26 · 2023: 15 · 2022: 24 · 2021: 27 · 2020: 30 · 2019: 33 · 2018: 46 · 2017: 46 · 2016: 41 · 2015: 24
- FWCI
- 3.49
- Type
- journal article
- Language
- en
- Open access
- green
- hdl.handle.net
- Locations
- Annual Review of Immunology (publishedVersion)
- PubMed (publishedVersion)
- Radboud Repository (Radboud University) (submittedVersion)
- Funders
- National Institutes of Health (CA-04-6934, 15614, AI‐15614)
- National Cancer Institute (CA 046934, P30CA046934)
- National Institute of Allergy and Infectious Diseases (AI‑15614)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (AR‑45584, R01AR045584)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Immunology and Microbiology › Immunology › Cytokine Signaling Pathways and Interactions
- Keywords
- caspase-1, neutrophil serine proteases, inflammatory cytokines, cytokine activation, host defense, inflammatory diseases
- MeSH terms
- Animals, Disease Susceptibility, Humans, Inflammation, Interleukin-1, Cytokines, Inflammation Mediators, Inflammasomes
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