Ask about this productRelated genes to: IL33 protein
- Gene:
- IL1RL1 NIH gene
- Name:
- interleukin 1 receptor like 1
- Previous symbol:
- -
- Synonyms:
- ST2, FIT-1, ST2L, ST2V, DER4, T1, IL33R
- Chromosome:
- 2q12.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-17
- Date modifiied:
- 2017-07-07
- Gene:
- IL33 NIH gene
- Name:
- interleukin 33
- Previous symbol:
- C9orf26
- Synonyms:
- DVS27, DKFZp586H0523, NF-HEV, IL1F11
- Chromosome:
- 9p24.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-12-18
- Date modifiied:
- 2014-11-19
Related products to: IL33 protein
Related articles to: IL33 protein
- Acute kidney injury (AKI) is a common and fatal complication of severe pneumonia, yet the mechanisms linking pulmonary inflammation to remote kidney injury remain poorly understood. Multicenter cohort data (n = 300) revealed that the incidence of severe pneumonia-associated AKI (SP-AKI) was 53.6%, with a mortality rate of 24.2%. SP-AKI was associated with elevated circulating levels of HMGB1, NETs, and IL-33. Murine experiments demonstrated that alveolar HMGB1 triggers the formation of IL-33-enriched NETs, which migrate to the kidney and activate tubular ST2/NF-κB signaling, driving inflammation and apoptosis. Genetic knockout of IL-33, ST2, or the NET-forming key enzyme PAD4, as well as pharmacological inhibition of HMGB1, IL-33, or NETs, all attenuated lung and kidney injury. Exogenous HMGB1 amplified NET-mediated IL-33 release, establishing a self-sustaining HMGB1/NET/IL-33 feed-forward loop. PAD4 deficiency completely blocked NET generation and disrupted HMGB1/IL-33 signaling. This study identified and validated a damage-associated molecular pattern-driven (DAMP-driven) HMGB1/NET/IL-33 signaling axis that mediates remote kidney injury in SP-AKI, redefining NETs from local effectors to cross-organ pathogenic carriers, thereby providing potential DAMP-targeted therapeutic avenues for SP-AKI. - Source: PubMed
Publication date: 2026/05/22
Ma MengqingZhang HaoDeng WeijuanDu XiaChen MengxingChen DaweiPan BinbinWang ZhaoweiChen TingChen CaimeiWan XinCao Changchun - Information is missing on the tissue cell expression patterns of interleukin IL-33 (IL-33) and splice variants of the IL-33 receptor ST2 in normal and COPD lungs. - Source: PubMed
Publication date: 2026/03/23
Andersson Cecilia KSiddhuraj PremkumarJönsson JimmieAhlgren JohanLindö CarolineNys Josquin AScott Ian CLindstedt SandraKolbeck RolandHumbles Alison ALutter RenéSabogal Piñeros Y SJonkers René ETufvesson EllenSandén CarolineCohen E SuzanneErjefält Jonas S - Depression remains a leading cause of global disability, yet its precise neurobiological underpinnings are incompletely understood. While inflammatory cytokines have been implicated in depressive pathology, the specific role of Interleukin-33 (IL-33) and its receptor ST2 in modulating microglial-mediated neuroinflammation has remained elusive. In this study, we reveal that deficiency of the IL-33/ST2 signaling axis in naive adult male mice selectively induces depression-like behaviors without impairing memory, motor coordination, or balance. This behavioral phenotype is mechanistically linked to heightened microglial activation, increased branching complexity, and exacerbated neuronal loss within the medial prefrontal cortex (mPFC) and dentate gyrus (DG). Furthermore, we demonstrate that IL-33 counteract LPS-induced microglial activation, nuclear translocation, and subsequent neuroinflammatory responses in vitro. Collectively, these findings delineate a novel neuroimmune pathway wherein IL-33/ST2 deficiency precipitates microglia-driven neuroinflammation, thereby contributing to depressive phenotypes. - Source: PubMed
Publication date: 2026/04/28
Wang HaoyuYang SiyuDai JiapeiZheng FangLuo YiZhao JiachenDu ELei KeLei JiawenLiu JinpengXiao YifanChen HuoyingSun Yan - Intrauterine adhesion (IUA) is a common complication following endometrial injury, characterized by endometrial fibrosis and partial or complete obliteration of the uterine cavity, severely affecting menstrual function and fertility in women of reproductive age. Recent studies have demonstrated that aberrant repair processes after endometrial injury involve complex inflammatory responses and immune regulation, among which macrophage polarisation imbalance plays a critical role in fibrosis progression. As a member of the IL-1 family, IL-33 can activate the MAPK signalling pathway through binding to its receptor ST2, participating in the regulation of macrophage polarisation; however, its specific mechanisms in the pathogenesis and progression of IUA remain unclear. This study aimed to investigate the mechanism by which the IL-33/ST2/MAPK signalling pathway contributes to endometrial fibrosis following endometrial injury, and to elucidate the molecular basis through which it promotes intrauterine adhesion (IUA) formation by regulating macrophage polarisation, thereby offering a potential target for clinical intervention. - Source: PubMed
Publication date: 2026/04/26
Li GuangfengXu FengjuanLuo SangJin YiranYuan LiweiYang XitangXuan TingtingLiu Dan - To investigate the proliferation and apoptosis of nucleus pulposus cells stimulated by IL-33, as well as the activation of the PI3K/AKT signaling pathway in these cells, and to determine whether this pathway is regulated by the IL-33/ST2 axis. - Source: PubMed
Publication date: 2026/04/21
Wang HaoranZhou PingChen YanruiLi YiLiu Jun