Ask about this productRelated genes to: IL33 antibody
- 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 antibody
Related articles to: IL33 antibody
- The dynamic interplay between pro- and anti-inflammatory cytokines plays a crucial role in regulating host immune responses. In our earlier study, we showed that Leishmania donovani-induced IL-33 destabilizes host cytokine dynamics by downregulating TNF-α and IL-12 and ensures intramacrophage parasite survival. Another pertinent host favorable proinflammatory cytokine is Il-1β, maturation of which depends on the activation of NLRP3 inflammasome complex. Our present study highlights that independent neutralization of IL-33 and its receptor ST2, resulted in elevated levels of NLRP3 both at messenger RNA and protein levels, along with increased levels of mature IL-1β. Reduced NLRP3 expression during infection was correlated with decreased protein levels of p65, the major subunit of NF-κB transcription factor complex. An unaltered transcript level of p65 in infected macrophages along with reduced protein expression suggested that post-translational modification and ubiquitination-mediated p65 degradation in the presence of IL-33 was found to be driven by the ubiquitin ligase SOCS1. Administration of IL-33-neutralizing antibody in infected mice resulted in enhanced expression of both p65 and NLRP3, along with increased production of TNF-α, IL-12, and IL-1β, suggesting that IL-33 regulates these cytokines through a shared intermediary, p65. Neutralizing IL-33 during infection led to a reduction in SOCS1 expression, and SOCS1 knockdown by targeted short hairpin RNA in infected mice restores p65 levels, reactivates NLRP3 expressions, and reduces parasite burden in the visceral organs. This study highlights the IL-33/SOCS1 pathway as a potential target for host-directed therapeutic strategies aimed at restoring protective immunity during chronic leishmaniasis. - Source: PubMed
Roy SouraviMandal MayumiBanerjee MadhurimaMadbhagat PratibhaChande AjitUkil Anindita - Soluble suppression of tumorigenicity 2 (sST2), a decoy receptor of interleukin-33 (IL-33), is involved in allergic inflammation and may serve as a biomarker in allergic rhinitis (AR). MicroRNA-223 (miR-223) has also been implicated in allergic inflammation. To investigate serum sST2 and miR-223 as potential biomarkers of disease activity and treatment-associated changes in patients with house dust mite (HDM)-induced moderate-to-severe allergic rhinitis (MSAR) undergoing sublingual immunotherapy (SLIT). This study included 54 patients with moderate-to-severe AR (MSAR) and 54 healthy controls (HC). Serum sST2, total IgE, HDM-specific IgE, and eosinophil counts were measured. Serum miR-223 relative expression was assessed using real-time PCR. Clinical severity was assessed using the total nasal symptom score (TNSS) and visual analogue scale (VAS). MSAR patients received SLIT for 6 months. Treatment response was defined as a ≥ 30% reduction in TNSS from baseline. Serum sST2 and miR-223 were significantly higher in MSAR patients than in healthy controls (p < 0.001). sST2 correlated positively with HDM-specific IgE and eosinophil counts and decreased significantly after six months of treatment (p < 0.001). Post-treatment sST2 was lower in responders, whereas baseline sST2 did not differ significantly between groups. ROC analysis showed good discrimination of MSAR from HC for sST2 (AUC = 0.933) and miR-223 (AUC ≈ 0.96). Serum sST2 and miR-223 show promising potential as candidate biomarkers of HDM-induced MSAR. The decrease in sST2 after treatment suggests its potential value for monitoring treatment-associated changes. Further studies are needed to validate these findings.Trial registration Retrospectively registered on ClinicalTrials.gov, registered at 25/2/ 2026, Identifier (NCT07436208). Registered at: https://clinicaltrials.gov/study/NCT07436208. - Source: PubMed
Publication date: 2026/09/08
Mokhtar Ghada AGebriel Manar GAbdelnour Hanim MSalah Abd El Azeem El Sayed MohamedHadhoud Ahmed NagyRoman Sylvia WMohamed Noura MostafaElGwad Asmaa Mohamed AbdIbraheem Ahmed A ANofal Hanaa AOmran Farida HMohammed Shrouk A - IL-33, an alarmin cytokine binding to IL1RL1 (ST2) receptor, plays a multifaceted role in cancer. Using an HPV16-E7 oncoprotein-mediated murine model of squamous intraepithelial hyperplasia, a pre-stage of squamous cell carcinoma (SCC), we characterised the interactions of hyperproliferative epithelial cells and immune cells regulated by IL-33 and IL1RL1. We show that basal epithelial cells in epithelial hyperplasia co-express IL-33 and genes involved in MHC class II antigen presentation and in epithelial stress response. Using spatial transcriptomics, we demonstrate that IL1RL1Foxp3Tregs are in close proximity to IL-33-expressing cells, in both the murine model and in human cervical intraepithelial neoplastic tissues. Cytoplasmic location of IL-33 is associated with its bioactivity, and we show that a subset of epithelial cells in epithelial hyperplasia contains high levels of cytoplasmic IL-33. Genetic deletion of the IL1RL1 gene led to partial rejection of HPV16-E7-expressing skin grafts, demonstrating that IL1RL1 plays a functional role in mediating immune suppression in epithelial hyperplasia. IL1RL1-deletion further led to a significant reduction in Tregs in epithelial hyperplasia. The IL1RL1 signalling pathway, therefore, represents a potential therapeutic target for intraepithelial hyperplasia and SCC. - Source: PubMed
Publication date: 2026/09/01
Zhou ChenhaoGonzalez Cruz JazminaTeoh Siok MinTran MinhGoh DeniseNarayanan DivyaaTan XiaoDang Thi Viet TrinhTuong Zewen KelvinGillinder KevinBashaw AbateWells James WFrazer Ian HNguyen QuanChen YuYu MeihuaChandra Janin - Interleukin-33 (IL-33) has long been categorized as a prototypical alarmin released upon cellular injury to initiate Th2-skewed immune responses. However, accumulating evidence from diverse kidney disease models and patient cohorts has unveiled a far more complex and contextually governed functionality. This review synthesizes recent advances to reframe the understanding of IL-33, positioning it not merely as a passive danger signal, but as an active and versatile rheostat of renal pathophysiology. The net effect of IL-33/ST2 signaling, whether tissue-protective or pro-inflammatory and fibrotic, is critically dictated by the disease microenvironment, encompassing the nature of the initial insult (e.g., ischemia-reperfusion, nephrotoxic agents, or autoimmune complexes), the phase of disease (acute versus chronic), and the local immune-parenchymal cell network. We delineate how the IL-33/ST2 axis differentially orchestrates key immune effectors, including group 2 innate lymphoid cells (ILC2s), macrophage polarization states, and T cell subsets with particular emphasis on regulatory T cells (Tregs). These interactions in turn shape divergent clinical outcomes, ranging from effective tissue repair and functional recovery to relentless inflammation and progressive fibrosis. By integrating findings across acute kidney injury, diabetic nephropathy, lupus nephritis, and IgA nephropathy, this review underscores the dual, context-dependent nature of IL-33 signaling. We further discuss its emerging potential as a stratified biomarker and a modifiable therapeutic target, and advocate for future strategies that precisely calibrate IL-33/ST2 activity according to specific pathological contexts, with the goal of achieving optimized and durable renal outcomes. - Source: PubMed
Publication date: 2026/08/14
Yang MeiMiao SuningYu MingliFu XiaoqingQin Xiaosong - Interleukin-33 (IL-33) and soluble ST2 (sST2) are critical regulators of tissue-derived inflammation, and their dysregulation is usually implicated in various inflammatory disorders. Despite this, how these circulating proteins behave over time in healthy individuals remains poorly defined. Therefore, defining reference concentrations in healthy cohorts is important for interpreting disease-associated changes attributed to these proteins. - Source: PubMed
Publication date: 2026/08/13
Anabe DeniseTeräsjärvi Johanna TBarkoff Alex-MikaelMertsola JussiHe Qiushui