IL1R2 _ CD121b Protein
- Known as:
- IL1R2 _ CD121b Protein
- Catalog number:
- 10111-H02H
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Smart Serology
- Gene target:
- IL1R2 _ CD121b Protein
Related genes to: IL1R2 _ CD121b Protein
- Gene:
- IL1R2 NIH gene
- Name:
- interleukin 1 receptor type 2
- Previous symbol:
- IL1RB
- Synonyms:
- CD121b
- Chromosome:
- 2q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1992-11-30
- Date modifiied:
- 2016-10-05
Related products to: IL1R2 _ CD121b Protein
Related articles to: IL1R2 _ CD121b Protein
- Osteoarthritis (OA) and intervertebral disc degeneration (IVDD) are debilitating musculoskeletal disorders driven by shared inflammatory pathologies, yet lack effective disease-modifying therapies. Pro-inflammatory macrophages are central to their pathogenesis, but their selective therapeutic modulation remains a major challenge. Here, we first used single-cell transcriptomics to identify a conserved, pathogenic interleukin-1β (IL-1β) macrophage signature fueled by a shared nuclear factor-κB (NF-κB)-inflammation axis in human OA and IVDD. We engineered a macrophage-biomimetic nanosystem (GM1-dMOF@PTL), a "doppelgänger" nanosystem designed for targeted cellular reprogramming. The platform consists of a Parthenolide (PTL)-loaded, lysosome-escaping metal-organic framework (MOF) core camouflaged with inflammatory macrophage membranes, with the IL-1β decoy receptor, interleukin-1 receptor type 2 (IL-1R2), overexpressed. This design enables a multi-pronged immunomodulatory strategy: the decoy receptor could neutralize extracellular IL-1β, while the macrophage-biomimetic surface facilitates homotypic targeting and preferential uptake by inflammatory macrophages. Upon internalization, the nanosystem potently suppresses the NF-κB/ NLR family pyrin domain containing 3 (N inflammasome axis, effectively disarming the cell's pyroptotic program. Crucially, local administration in mouse models preserved disc and cartilage integrity, resolved inflammation, and provided sustained alleviation of pain hypersensitivity. This study presents a unified, disease-modifying nanotherapeutic strategy that targets a shared cellular driver by synergistically neutralizing inflammatory signals and reprogramming pathogenic immune cells to attenuate both spine and joint degeneration. - Source: PubMed
Publication date: 2026/08/20
Li FudongZhang BinZhang ZhiqiuZheng BingHan LinhuiYan ChenLi JialinSun KaiqiangZhao TianyiShi Jiangang - Sepsis remains difficult to diagnose since blood culture has low sensitivity and current biomarkers lack sufficient specificity. We sought to identify robust diagnostic and therapeutic targets for neonatal sepsis through an integrated bioinformatics and experimental workflow. - Source: PubMed
Publication date: 2026/08/12
Li JunjieXiu GuanghuiLiu PingChen XianzhongZhou KailvYang Yunfeng - Coronavirus disease 2019 (COVID-19) is characterized by dysregulated immune responses and excessive inflammation, contributing to severe disease and mortality. Interleukin-1 receptor type 2 (IL1R2), a decoy receptor for interleukin-1 (IL-1), regulates inflammatory responses; however, its cellular distribution and clinical significance in COVID-19 remain unclear. - Source: PubMed
Publication date: 2026/08/11
Yang YiyingYu FangLi MuyuanMa HaoZhang HualiXiao XianzhongCheng Liqin - Neonatal sepsis (NS) is one of the leading causes of neonatal mortality. The nonspecific clinical manifestations and the limited timeliness of existing biomarkers (such as C-reactive protein) highlight the urgent need for highly accurate diagnostic tools. Neutrophils, as key effector cells of innate immunity, are closely involved in the progression of NS. This study integrated training (GSE69686) and validation (GSE25504) datasets from the GEO database. Neutrophil infiltration characteristics were analyzed utilizing CIBERSORT, and weighted gene co-expression network analysis (WGCNA) was introduced to determine neutrophil-related co-expression modules. Three machine learning algorithms-LASSO, SVM-RFE, and RF-were implemented to cross-screen core diagnostic genes. A combined diagnostic model was distributed based on these genes. NetworkAnalyst was utilized to predict miRNA-TF regulatory networks, and GSVA was conducted to interpret biological functions. Three algorithms identified IL1R2 and METTL7B as core diagnostic genes; the model showed strong reliability. IL1R2 high expression correlated with reduced CD8 T cells, regulatory T cells, and neutrophils (<0.05). METTL7B high expression linked positively to B cells and negatively to NK cells/neutrophils. The two genes synergistically cause immune cell dysfunction. Six miRNAs and 15 transcription factors (e.g., NFKB1/RELA, STAT3) regulating these genes were found, involved in inflammation and metabolic reprogramming. Integrating neutrophil infiltration and triple-machine-learning, this study first proposed an IL1R2/METTL7B two-gene panel. The model had high accuracy and generalizability, potentially contributing to NS pathogenesis via immune dysfunction and metabolic reprogramming, supporting rapid diagnostics and targeted interventions. - Source: PubMed
Publication date: 2026/03/19
Chen QibingChen JiandongZhong Ronghua - Glioblastoma (GBM) is an aggressive and lethal brain tumor marked by profound local and systemic immune dysfunction. Despite evidence of peripheral immune impairment, the clinical relevance of these alterations for diagnostic or therapeutic purposes remains poorly defined. - Source: PubMed
Publication date: 2026/07/16
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