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
- 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 - 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 - The polarization of naive CD4+ T cells into Th2 cells is initiated in lymphoid organs and completed as the cells become tissue resident, where they express ST2, the receptor for the alarmin interleukin (IL)-33, which may be a key signal for tissue integration. Cellular metabolic requirements associated with this transition remain poorly understood. To address this, we compared the response of lymphoid tissue (LT) Th2 cells from helminth parasite-infected mice to stimulation by IL-33 versus through the T cell receptor via anti-CD3/CD28. We found that IL-33, but not anti-CD3/CD28, induced the development of tissue-resident like Th2 cells expressing ST2. This was associated with IL-33 induced changes in arginine metabolism linked to mTORC1 activation and polyamine synthesis, which were required for the development of tissue-resident like Th2 cells. Furthermore, IL-33 induced transcriptional changes in genes involved in chemotaxis and cell adhesion that may be critical for tissue integration. Our findings provide insights into adaptations of Th2 cells responding to tissue-integration cues and more broadly support the view that IL-33 promotes the expression of the transcriptional program associated with tissue residency of GATA3-expressing cells in adipose and possibly other tissues. - Source: PubMed
Kania Anna KSanin David EGu XinyueGidley MiaKokosinski ErykSmith AllenPearce ErikaPearce Edward J - This study aimed to examine the role of the interleukin-33 (IL-33)/suppression of tumorigenicity 2 (ST-2) signaling pathway in hepatic fibrogenesis within the microenvironment of alveolar echinococcosis (AE). The therapeutic efficacy and immunomodulatory effects of concurrent IL-33/ST-2 pathway inhibition and albendazole (ABZ) treatment were also evaluated. - Source: PubMed
Publication date: 2026/04/03
Cheng Shi-LeiMa Xiu-MeiWu Bin-JieYang Yu-XuanFan Hai-Ning - The IL-33/ST2 pathway is important as part of the type 2 immune response against helminth infections. Mast cells express the highest levels of the IL-33 receptor subunit ST2 of any immune cell, and mast cells can mediate type 2 immune inflammation; however, the role of IL-33-driven mast cell responses in helminth infection is poorly understood. We sought to determine the role of mast cell ST2 expression during Heligmosomoides polygyrus bakeri (Hpb) infection by generating mast cell conditional ST2 knockout (MCPT5 × ST2, cKO) mice. These mice have normal frequencies of mast cells at steady state but show specific and strong (albeit incomplete) knockdown of ST2 expression on mast cells. On Hpb infection, faecal egg and adult worm burden were similar between cKO and littermate controls, as were mast cell degranulation markers, serum IgE and goblet cell hyperplasia. Therefore, we conclude that mast cell ST2 does not play a dominant role in Hpb infection. To further investigate the immune response to infection in cKO and littermate controls, transcriptomic and proteomic changes were assessed in duodenal tissues in infected versus naïve mice in cKO and control mice. Minimal transcriptomic and proteomic changes were seen between genotypes, whereas substantial changes were seen between naïve and infected mice, regardless of genotype. Hpb infection induced local increases at the transcript and protein level for mast cell proteases (MCPT1 and MCPT2), resistin-like molecules (RELMα and RELMβ) and markers such as the phospholipase PLA2G4C and the pore-forming protein gasdermin C. Bulk proteomic analysis was also searched against the Hpb genome to identify Hpb proteins present in the duodenal tissues. A list of 60 Hpb proteins of interest was identified in infected duodenal samples, of which 18 contain a signal peptide and are present in the excretory/secretory products of Hpb (HES) (likely secretory products including immunomodulatory proteins); 28 proteins are present in HES but do not contain a signal peptide (likely excretory products); and 14 proteins are not present in HES (likely proteins present in the remnants of Hpb within the duodenum). This work thus provides datasets for changes in the mouse intestine due to Hpb infection, at both the transcript and protein level, as well as a dataset of Hpb proteins detectable in the mouse duodenum at day 14 of infection. - Source: PubMed
Ong Nicole W PHodge Suzanne HBaker Christa PSmyth Danielle JFrangova TaniaMcSorley Henry J