Relevant bibliographies by topics / IL1RL1 (ST2)

Academic literature on the topic 'IL1RL1 (ST2)'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "IL1RL1 (ST2)"

1

Ramirez-Carrozzi, Vladimir, Amy Dressen, Patrick Lupardus, Brian Yaspan, and Rajita Pappu. "Functional analysis of protective IL1RL1 variants associated with asthma risk (CCR6P.215)." Journal of Immunology 194, no. 1_Supplement (May 1, 2015): 187.2. http://dx.doi.org/10.4049/jimmunol.194.supp.187.2.

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Abstract GWAS studies have identified polymorphisms in both IL33 and IL1RL1, the gene encoding ST2, the high affinity chain of the IL-33 receptor, that associate with asthma susceptibility. We identified amino acid changing variants in IL1RL1 associating with asthma incidence and found these SNPs to be protective from asthma risk in our study population. These variants result in coding changes to the intracellular region of ST2, which contains the TIR domain of the receptor that is critical for signaling downstream of IL-1 cytokine family and TLRs. Mutations or deletions to this region can inhibit ligand-induced responses. IL-33-mediated dimerization of ST2 and IL-1RAcP promotes TIR-TIR domain interaction and recruitment of the adaptor molecule MyD88 leading to AP-1 and NF-kB activation. IL-33 responses were diminished in cell lines expressing all 4 IL1RL1 missense variants. To further elucidate how this haplotype could affect IL-33 activity, we compared IL-33 activity and ST2 expression between donors carrying either haplotype. We observed reduced IL-33 mediated IL-8 secretion from purified blood eosinophils derived from individuals carrying the protective haplotype. We also observed greater soluble ST2 expression in these individuals. Our results provide a link between the genetic predisposition to asthma and IL-33 mediated responses. Given IL-33 promotes Th2 immunity, perturbations that diminish this response may provide protection from asthma risk.
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Dale, Mark, and Martin J. H. Nicklin. "Interleukin-1 Receptor Cluster: Gene Organization ofIL1R2, IL1R1, IL1RL2(IL-1Rrp2),IL1RL1(T1/ST2), andIL18R1(IL-1Rrp) on Human Chromosome 2q." Genomics 57, no. 1 (April 1999): 177–79. http://dx.doi.org/10.1006/geno.1999.5767.

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Ho, Jennifer E., Wei-Yu Chen, Ming-Huei Chen, Martin G. Larson, Elizabeth L. McCabe, Susan Cheng, Anahita Ghorbani, et al. "Common genetic variation at the IL1RL1 locus regulates IL-33/ST2 signaling." Journal of Clinical Investigation 123, no. 10 (September 3, 2013): 4208–18. http://dx.doi.org/10.1172/jci67119.

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Valeff, Natalin Jimena, Maria Silvia Ventimiglia, Florencia Quadrana, and Federico Jensen. "ST2-expressing B1 B cells acquire an anti-inflammatory capacity during pregnancy in mice." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 235.14. http://dx.doi.org/10.4049/jimmunol.204.supp.235.14.

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Abstract In the context of pregnancy, it is known that IL-33 induces the production of anti-inflammatory molecules by decidual B1 cells, protecting against preterm birth (PTB) in human and mouse. We have previously showed that expression of IL-33 receptor, Il1rl1 (ST2) is significantly upregulated in splenic B cells during mid pregnancy, predominantly in B1 cell subset. Furthermore, using an LPS induced PTB mouse model, we observed increased numbers of splenic and decidual ST2-expressing B1 cells in the acute phase of PTB as compared to term pregnant females. We aimed to investigate here the anti-inflammatory properties of ST2-expressing B1 cells during pregnancy. Total splenocytes from pregnant (P) and non-pregnant (NP) mice were isolated and cultured for 24h with/without LPS (10 μgr/ml), ST2 expression and cytokine production by ST2+ B1 cells was evaluated by flow cytometry. B1 cells from P mice stimulated with LPS showed significantly higher levels of ST2 expression. ST2+ B1 cells produced significantly higher levels of IL-10 and significantly lower levels of TNF-α and IL-17 as compared to ST2+ B1 cells from NP mice. In a separate project in our laboratory we demonstrated that prophylactic treatment with probiotic Lactobacillus kefiri prevented LPS-induced PTB in mice. Interestingly, we observed that numbers of splenic and decidual ST2-expressing B1 cells were increased in L. kefiri treated mice that were protected against LPS-induced PTB. Our data strongly suggest an anti-inflammatory capacity of ST2-expressing B1 cells during gestation, presumably to ensure pregnancy wellbeing and prevent inflammation induced PTB.
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Rasheed, Kashif, Ugo Moens, Benedetta Policastro, John Inge Johnsen, Virve Koljonen, Harri Sihto, Weng-Onn Lui, and Baldur Sveinbjørnsson. "The Merkel Cell Polyomavirus T-Antigens and IL-33/ST2-IL1RAcP Axis: Possible Role in Merkel Cell Carcinoma." International Journal of Molecular Sciences 23, no. 7 (March 28, 2022): 3702. http://dx.doi.org/10.3390/ijms23073702.

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Merkel cell polyomavirus (MCPyV) is a causal factor in Merkel cell carcinoma (MCC). The oncogenic potential is mediated through its viral oncoproteins large T-antigen (LT) and small T-antigen (sT). Cytokines produced by tumor cells play an important role in cancer pathogenesis, and viruses affect their expression. Therefore, we compared human cytokine and receptor transcript levels in virus positive (V+) and virus negative (V−) MCC cell lines. Increased expression of IL-33, a potent modulator of tumor microenvironment, was observed in V+ MCC cell lines when compared to V− MCC-13 cells. Transient transfection studies with luciferase reporter plasmids demonstrated that LT and sT stimulated IL-33, ST2/IL1RL1 and IL1RAcP promoter activity. The induction of IL-33 expression was confirmed by transfecting MCC-13 cells with MCPyV LT. Furthermore, recombinant human cytokine domain IL-33 induced activation of MAP kinase and NF-κB pathways, which could be blocked by a ST2 receptor antibody. Immunohistochemical analysis demonstrated a significantly stronger IL-33, ST2, and IL1RAcP expression in MCC tissues compared to normal skin. Of interest, significantly higher IL-33 and IL1RAcP protein levels were observed in MCC patient plasma compared to plasma from healthy controls. Previous studies have demonstrated the implication of the IL-33/STL2 pathway in cancer. Because our results revealed a T-antigens-dependent induction of the IL-33/ST2 axis, IL-33/ST2 may play a role in the tumorigenesis of MCPyV-positive MCC. Therefore, neutralizing the IL-33/ST2 axis may present a novel therapeutic approach for MCC patients.
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Griesenauer, Brad, Jilu Zhang, Abdulraouf M. Ramadan, and Sophie Paczesny. "Deficiency of MyD88 signaling in CD4 Tconvs increases Tregs suppression through loss of ST2 signaling." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 82.12. http://dx.doi.org/10.4049/jimmunol.198.supp.82.12.

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Abstract Acute graft-versus-host disease (aGVHD) hinders the efficacy of allogeneic hematopoietic cell transplantation (allo-HCT). We found that plasma soluble suppression of tumorigenicity 2 (sST2) predicted GVHD-related mortality in allo-HCT patients. ST2 signals through the adapter protein MyD88. Lack of MyD88 in CD4 Tconvs has been shown to decrease ovalbumin or a peptide to the haplotype H2b stimulated Th1/Th17 cells via the IL-1R. Thus, we hypothesized that absence of MyD88 signaling would protect against aGVHD through IL-1R, ST2, or both. We found that knocking out MyD88 in the donor T cells protected against aGVHD while recipients of IL-1R−/− donor T cells showed no difference. We found that the aGVHD protection was entirely driven by MyD88−/− CD4 T cells. There were no differences in proliferation, apoptosis, or migration in WT or MyD88−/− CD4 T cells. We next explored the cell-intrinsic role of MyD88−/− Tconvs and Tregs. We did not find a difference in survival in aGVHD models with MyD88−/− Tconvs or MyD88−/− Tregs. However, use of MyD88−/− Tconvs with WT or MyD88−/− Tregs ameliorated aGVHD. We hypothesized that this was mediated by lack of ST2 on donor Tconvs. Recipients of ST2−/− Tconvs with WT or ST2−/− Tregs lowered aGVHD mortality, mirroring MyD88−/− Tconvs. Transcriptome analysis comparing 10 days post-HCT CD4 T cells from MyD88−/− versus WT recipients showed lower levels of Irak1, Il1rl1 (gene of ST2), Ifng, Csf2, Stat5, and Jak2 as well as decreased systemic plasma sST2 and IFN-γ levels. Our data suggests that Tregs suppression from lack of MyD88 signaling in Tconvs during alloreactivity uses the ST2 but not the IL-1R pathway, possibly by different antigen stimulation. MyD88 represents an aGVHD therapeutic target sparing Treg function.
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Tago, Kenji, Satoshi Ohta, Megumi Funakoshi-Tago, Chihiro Aoki-Ohmura, Jitsuhiro Matsugi, Shin-ichi Tominaga, and Ken Yanagisawa. "STAT3 and ERK pathways are involved in cell growth stimulation of the ST2/IL1RL1 promoter." FEBS Open Bio 7, no. 2 (January 19, 2017): 293–302. http://dx.doi.org/10.1002/2211-5463.12192.

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8

Bahrij, D. A. "Clinical significance of single nucleotide missense-mutation rs950880 of the IL1RL1 gene in patients with essential hypertension." Biomedical and Biosocial Anthropology, no. 42 (March 27, 2021): 52–56. http://dx.doi.org/10.31393/bba42-2021-09.

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Modern cardiology requires the search for specific pathogenetically involved gene mutations, the consequences of which can be considered in the management of patients with hypertension. Scientists are targeting C/A polymorphism at the rs950880 position, which is associated with tissue expression of the IL1RL1 gene and the plasma level of soluble ST2 – a new biomarker in the diagnosis of cardiovascular disease. The aim of the study was to evaluate the association of rs950880 polymorphism of the IL1RL1 gene and the state of central and intracardiac hemodynamics in men with essential hypertension (EН) of varying severity, residents of the Podillia region of Ukraine. 170 men who met the inclusion criteria were examined according to a standard protocol, which included clinical, laboratory and instrumental examinations in accordance with current recommendations. The subjects were divided into a control group of 70 men without cardiovascular disease and a study group of 50 men with asymptomatic EН and 50 people with EH complicated by IIA stage chronic heart failure (CHF). Genotyping of SNP rs950880 of the IL1RL1 gene was performed using an allele-specific polymerase chain reaction. All men in the control group and the study group underwent echocardiography with Doppler according to the standard protocol. Statistical processing of the obtained results was performed in the package Statistica 12.0 using conjugation tables analysis, analysis of variance. It was found that among men living in Vinnytsia, Ukraine, carriers of СС and CA SNP rs950880 of the IL1RL1 gene dominate (42.35 % and 45.30 % of individuals, respectively), AA homozygotes are significantly less common (12.53 %, p<0.05). Men without cardiovascular diseases and patients with EH do not differ significantly in the frequency of different variants of the genotype of the studied gene. C\A polymorphism is not associated with the risk of EН. The homozygotes AA with EH have a significantly lower LV myocardial mass index (LVMMI) (69.14±6.90 g/m2.7, compared with homozygotes CC – 75.42±2.54 g/m2.7, and heterozygotes CA – 76.96±3.18 g/m2.7, p<0.05). Among the carriers of the C allele, an "unfavorable" EН phenotype is mainly formed in the form of a high risk of LV hypertrophy (OR=11.36, 95 % СI=0.63-24.76, χ2=14.32, p=0.0008). Homozygotes AA in the rs950880 locus of the IL1RL1 gene, on the contrary, have a low probability of developing LV hypertrophy (OR=0.80, 95 % SI=0.02-0.42, χ2=14.32, p=0.0008) and its preserved systolic function. Thus, the SNP rs950880 of the IL1RL1 gene is not associated with the risk of EH or its severity in residents of Vinnytsia, Ukraine. Carriage of the C allele is accompanied by the formation of an "unfavorable" EH phenotype with a significantly high risk of LV hypertrophy.
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Baba, Yosuke, Keiko Maeda, Takuya Yashiro, Eisuke Inage, Frangois Niyonsaba, Mutsuko Hara, Ryuyo Suzuki, et al. "Involvement of PU.1 in Mast Cell/Basophil-Specific Function of the Human IL1RL1/ST2 Promoter." Allergology International 61, no. 3 (2012): 461–67. http://dx.doi.org/10.2332/allergolint.12-oa-0424.

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10

Maywald, Rebecca L., Stephanie K. Doerner, Luca Pastorelli, Carlo De Salvo, Susan M. Benton, Emily P. Dawson, Denise G. Lanza, et al. "IL-33 activates tumor stroma to promote intestinal polyposis." Proceedings of the National Academy of Sciences 112, no. 19 (April 27, 2015): E2487—E2496. http://dx.doi.org/10.1073/pnas.1422445112.

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Tumor epithelial cells develop within a microenvironment consisting of extracellular matrix, growth factors, and cytokines produced by nonepithelial stromal cells. In response to paracrine signals from tumor epithelia, stromal cells modify the microenvironment to promote tumor growth and metastasis. Here, we identify interleukin 33 (IL-33) as a regulator of tumor stromal cell activation and mediator of intestinal polyposis. In human colorectal cancer, IL-33 expression was induced in the tumor epithelium of adenomas and carcinomas, and expression of the IL-33 receptor, IL1RL1 (also referred to as IL1-R4 or ST2), localized predominantly to the stroma of adenoma and both the stroma and epithelium of carcinoma. Genetic and antibody abrogation of responsiveness to IL-33 in the ApcMin/+ mouse model of intestinal tumorigenesis inhibited proliferation, induced apoptosis, and suppressed angiogenesis in adenomatous polyps, which reduced both tumor number and size. Similar to human adenomas, IL-33 expression localized to tumor epithelial cells and expression of IL1RL1 associated with two stromal cell types, subepithelial myofibroblasts and mast cells, in ApcMin/+ polyps. In vitro, IL-33 stimulation of human subepithelial myofibroblasts induced the expression of extracellular matrix components and growth factors associated with intestinal tumor progression. IL-33 deficiency reduced mast cell accumulation in ApcMin/+ polyps and suppressed the expression of mast cell-derived proteases and cytokines known to promote polyposis. Based on these findings, we propose that IL-33 derived from the tumor epithelium promotes polyposis through the coordinated activation of stromal cells and the formation of a protumorigenic microenvironment.
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Conference papers on the topic "IL1RL1 (ST2)"

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Klein, S., I. Nolte, E. M. Packeiser, M. Sehn, P. Lietz, J. Raue, J. Treese, and J. P. Bach. "Neuartige kardiale Biomarker Galectin-3 und ST2 (IL1RL1) bei Hunden mit einer Mitralklappenerkrankung." In 28. Jahrestagung der FG „Innere Medizin und klinische Labordiagnostik“ der DVG (InnLab) – Teil 2: Poster. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0039-1700930.

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Klein, S., I. Nolte, E. M. Packeiser, N. Iwanuk, K. Rumstedt, J. Treese, F. Weiner, and J. P. Bach. "Evaluation der kardialen Biomarker Galectin-3 und ST2 (IL1RL1) bei Patienten mit beginnender degenerativer Mitralklappenerkrankung (CHIEF B)." In 27. Jahrestagung der FG „Innere Medizin und klinische Labordiagnostik“ der DVG (InnLab) – Teil 1. Georg Thieme Verlag KG Stuttgart · New York, 2019. http://dx.doi.org/10.1055/s-0039-1678431.

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