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Role of IL-33 in inflammation and disease
Open accessAbstract
Interleukin (IL)-33 is a new member of the IL-1 superfamily of cytokines that is expressed by mainly stromal cells, such as epithelial and endothelial cells, and its expression is upregulated following pro-inflammatory stimulation. IL-33 can function both as a traditional cytokine and as a nuclear factor regulating gene transcription. It is thought to function as an 'alarmin' released following cell necrosis to alerting the immune system to tissue damage or stress. It mediates its biological effects via interaction with the receptors ST2 (IL-1RL1) and IL-1 receptor accessory protein (IL-1RAcP), both of which are widely expressed, particularly by innate immune cells and T helper 2 (Th2) cells. IL-33 strongly induces Th2 cytokine production from these cells and can promote the pathogenesis of Th2-related disease such as asthma, atopic dermatitis and anaphylaxis. However, IL-33 has shown various protective effects in cardiovascular diseases such as atherosclerosis, obesity, type 2 diabetes and cardiac remodeling. Thus, the effects of IL-33 are either pro- or anti-inflammatory depending on the disease and the model. In this review the role of IL-33 in the inflammation of several disease pathologies will be discussed, with particular emphasis on recent advances.
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“By acting on T-cells and innate immune cells (Miller, 2011; Brownell and Polyak, 2013), CXCL10 and IL-33 might contribute to the amplification of inflammatory responses.”
From Model Based Targeting of IL-6-Induced Inflammatory Responses in Cultured Primary Hepatocytes to Improve Application of the JAK Inhibitor Ruxolitinib (2017) · cites this paper as Miller, 2011
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Metadata
- Authors
- Miller, A. M.
- Affiliations
- University of Glasgow (GB)
- Corresponding author
- Miller, Ashley M
- ORCID
- Miller, Ashley M
- Venue
- Journal of Inflammation
- Published
- 2011
- Volume
- 8
- Issue
- 1
- Pages
- 22
- ISSN
- 1476-9255 (ISSN-L)
- PMC
- PMC3175149
- OpenAlex
- W2137520462
- Cited by
- 481
- References
- 124
- Citations by year
- 2026: 18 · 2025: 21 · 2024: 27 · 2023: 39 · 2022: 27 · 2021: 32 · 2020: 37 · 2019: 31 · 2018: 28 · 2017: 48 · 2016: 40 · 2015: 42 · 2014: 33 · 2013: 27 · 2012: 25
- FWCI
- 12.77
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Journal of Inflammation (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- ENLIGHTEN (Jurnal Bimbingan dan Konseling Islam) (acceptedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- British Heart Foundation (FS/08/035/25309)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › IL-33, ST2, and ILC Pathways
- Life Sciences › Immunology and Microbiology › Immunology › Cytokine Signaling Pathways and Interactions
- Life Sciences › Immunology and Microbiology › Immunology › Mast cells and histamine
- Keywords
- IL-33, IL-1 superfamily, IL-1 receptor accessory protein, alarmins, Th2 cells, asthma, atopic dermatitis, anaphylaxis, atherosclerosis, obesity, type 2 diabetes, cardiac remodeling, inflammation, innate immunity
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