Ask about this productRelated genes to: IL18R1 Blocking Peptide
- Gene:
- IL18R1 NIH gene
- Name:
- interleukin 18 receptor 1
- Previous symbol:
- -
- Synonyms:
- IL1RRP, IL-1Rrp, CD218a
- Chromosome:
- 2q12.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-17
- Date modifiied:
- 2016-10-05
Related products to: IL18R1 Blocking Peptide
Related articles to: IL18R1 Blocking Peptide
- Neuroinflammation is a key process that shapes tumor progression and cellular stress responses. While pro-inflammatory signaling components amplify these responses, IL-37a functions as an endogenous suppressor that limits inflammation. Melittin is a bioactive peptide with cytotoxic and immunomodulatory properties; however, its effects on IL-37a-centered immune regulation in neuroblastoma cells remain unclear. SH-SY5Y neuroblastoma cells were treated in vitro with melittin at concentrations of 1-32 µM for 24 and 48 h. Cell viability was assessed using the MTT assay. Expression levels of selected genes related to inflammation and extracellular matrix were analyzed by qRT-PCR. Targeted gene expression data were further used for protein-protein interaction network analysis, pathway enrichment analyses, and multivariate statistical approaches. In addition, potential interactions between melittin and STAT3 or IL-1R8 were evaluated by molecular docking, and ADMET properties were predicted. Melittin induced dose- and time-dependent cytotoxicity in SH-SY5Y cells, with an IC value of 16 µM at 24 h. Melittin treatment led to a significant increase the expression of IL-37a, IL-18R1, and IL-1R8, while suppressing NF-κB, STAT3, MyD88, and Smad3. Caspase-1 expression was elevated, suggesting modulation of inflammation-associated cell death pathways. Extracellular matrix remodeling was differentially regulated, with increased MMP-2 and decreased MMP-9 expression. Multivariate analyses revealed a treatment-specific gene expression pattern. Molecular docking analyses suggested potential interactions between melittin and STAT3 or IL-1R8, while ADMET analysis indicated limited permeability and certain safety constraints. Melittin may emerge as a molecule that modulates inflammation-related gene expression in neuroblastoma cells and may be associated with IL-37a-related regulatory responses. These findings suggest that melittin could act as a potential modulator of inflammation-associated signaling pathways. - Source: PubMed
Publication date: 2026/06/09
Ertan BerkayYalcinkaya TugbaErcan ElifCarhan Ahmet - Species differ markedly in how they regulate immune responses, yet the molecular basis of this variation remains incompletely understood. Here, we characterize an underexplored regulatory mechanism of the pro-inflammatory IL-18 pathway, centered on a truncated isoform with striking species-specific expression differences. This isoform, , derives from an ancient LINE2 retrotransposon insertion that provides an intronic polyadenylation signal, producing a receptor that lacks the intracellular signaling domain. Using RNA sequencing across nine mammals, we find that although this cis-regulatory element is broadly conserved, robust expression is species- and tissue-restricted: bats and mice express it at high levels, particularly in barrier tissues (lung, skin, intestine), whereas most other species, including humans, show little or no expression. Functionally, IL18R1-Short dampens IL-18-induced NFκB signaling in human, mouse, and bat systems, and knockdown of the mouse ortholog enhances IL-18-driven immune and inflammatory gene expression in mouse T cells. Together, these results identify IL18R1-Short as a transposable element-derived decoy receptor and highlight alternative transcription as a source of species-specific immune regulation. - Source: PubMed
Publication date: 2026/05/26
Ordonez Andrea DAllen HollySanford LynnIvancevic AtmaAgyepong AshleyChaw MiaBridges James PSchountz TonyChuong Edward B - Acute respiratory failure (ARF) is a heterogeneous syndrome in which early differentiation between infection-related and non-infection-related etiologies remains challenging. This study aimed to characterize the inflammatory profile of type I ARF and identify candidate biomarkers associated with the infection-related type I ARF. - Source: PubMed
Ren KairuiXu JiatongWang YaLi YanZhu Huadong - Psoriasis is an immune-mediated inflammatory disease with a genetic component, characterized by dysregulation of cytokine signaling and activation of T lymphocytes. This study investigated genetic variants associated with psoriasis, psoriatic arthritis (PsA), and response to tumor necrosis factor alpha (TNF-α) inhibitors (adalimumab, infliximab, and etanercept) in a Russian cohort. A genome-wide association study (GWAS) was conducted in 1026 psoriasis patients and 9212 controls using Infinium Global Screening Array-24 v3.0 microarrays. Exploratory analyses of treatment response ( = 48) and PsA ( = 96) were performed without covariate adjustment or explicit modeling of population structure. Polygenic risk scores (PRS) were derived from internally estimated effect sizes in a split-sample design. The GWAS replicated a robust association in the major histocompatibility complex (MHC) region (rs12189871 near , = 3.2 × 10, OR = 2.99 [2.59-3.45]). Additional loci included variants in and . Nominal signals were observed for / in treatment response (including rs17027071) and for and in PsA; these findings remain exploratory. PRS demonstrated moderate predictive performance (AUC = 0.6355) and should be interpreted with caution given the study design. Overall, the results highlight a strong MHC signal in psoriasis, while findings for PsA and treatment response remain hypothesis-generating and require independent validation. - Source: PubMed
Publication date: 2026/05/15
Karamova Arfenya EBuianova Anastasiia AVorontsova Anastasiia AKubanov Alexey A - : Small cell lung cancer (SCLC) carries a dismal prognosis with limited biomarkers for risk stratification. This study aimed to identify circulating prognostic biomarkers. : We prioritized SCLC risk-associated genes using Summary-data-based Mendelian Randomization of pQTL/eQTL, differential expression, and weighted gene co-expression network analysis. Five machine learning approaches were compared to develop a diagnostic model based on , , and , trained on GSE149507 and validated in GSE60052. We conducted single-cell transcriptomic analysis using public datasets (GSE150766 and GSE279570) and peripheral blood mononuclear cells (PBMCs) from our extensive-stage cohort. Finally, prioritizing the lead candidate IL18R1, we enrolled a prospective clinical cohort to assess its prognostic utility. A LASSO-Cox prognostic model incorporating plasma IL18R1 and clinical variables was internally validated (7:3 split) for progression-free survival (PFS) prediction. : Integrative multi-omics identified , , and as SCLC-protective genes. Elastic Net machine learning identified a two-gene predictive signature ( and ) with robust diagnostic accuracy. Single-cell RNA sequencing revealed the predominant downregulation of , , and in T cells and alveolar type II cells from SCLC patients. PBMC analysis further supported downregulation in CD8 T cells, NK cells, and dendritic cells. In an independent prospective cohort ( = 300), lower plasma IL18R1 levels were independently associated with shorter PFS (HR = 0.997 per unit increase; 95% CI: 0.995-0.999; and = 0.003), with time-dependent AUCs of 0.77-0.86. Performance in limited-stage disease was inconsistent and requires further validation. A prognostic model incorporating plasma IL18R1 and 11 clinical parameters stratified patients into distinct risk groups (HR = 5.19), showing a strong discriminative ability in extensive-stage SCLC. : We identified , , and as protective factors against SCLC progression. Integration of plasma IL18R1 with clinical parameters provides a prognostic tool for extensive-stage SCLC. - Source: PubMed
Publication date: 2026/05/15
Hu ShengjuanLi SicongCui YiyuanWang YingChen LuyaoZhang XiyuanHou LiFeng Li