IL4R _ IL4Ra _ CD124 Antibody
- Known as:
- IL4R _ IL4Ra _ CD124 Antibody
- Catalog number:
- 10402-RP01
- Product Quantity:
- 200
- Category:
- -
- Supplier:
- Smart Serology
- Gene target:
- IL4R _ IL4Ra CD124 Antibody
Related genes to: IL4R _ IL4Ra _ CD124 Antibody
- Gene:
- IL4R NIH gene
- Name:
- interleukin 4 receptor
- Previous symbol:
- -
- Synonyms:
- CD124
- Chromosome:
- 16p12.1
- Locus Type:
- gene with protein product
- Date approved:
- 1990-07-06
- Date modifiied:
- 2017-07-07
Related products to: IL4R _ IL4Ra _ CD124 Antibody
Related articles to: IL4R _ IL4Ra _ CD124 Antibody
- The core pathological features of Alzheimer's disease (AD) include Aβ plaques and neurofibrillary tangles, which collectively drive the neurodegenerative process. Meanwhile, the phagocytic function of microglia plays a dual role in AD: it attempts to clear pathological proteins such as Aβ, but its chronic activation may also exacerbate neuroinflammation and synaptic damage. This study integrated microarray data from AD cohorts in the Gene Expression Omnibus (GEO) database. Through differential expression analysis, protein-protein interaction network construction, and three machine learning algorithms (Least Absolute Shrinkage and Selection Operator, Support Vector Machine-Recursive Feature Elimination, and Extreme Gradient Boosting), key microglial phagocytosis-related signature genes were identified. Diagnostic models were subsequently developed and validated, with further investigation of immune infiltration patterns, regulatory networks, and molecular subtypes. Based on comprehensive analysis, this study identified five core signature genes (HLA-DPA1, IL4R, ITGAM, SPP1, TNFRSF1B) that form a highly accurate diagnostic model validated in independent cohorts. Immune infiltration analysis revealed significant increases in neutrophils and M2 macrophages in AD brains, with these genes showing strong correlations with immune cell abundance. The study further identified two molecular subtypes with distinct immune features, constructed regulatory networks, and predicted potential therapeutics including Tamibarotene. By integrating transcriptomics and machine learning, this study identifies key molecular features of microglial phagocytosis in AD, providing a novel diagnostic framework and insights into the immune mechanisms of the disease. - Source: PubMed
Chang HuiminLiu YunYang XiaojunHan Yanqing - Traditionally associated with Th17-mediated pathways, palmoplantar pustulosis (PPP) is a persistent inflammatory dermatosis limited to the palms and soles. However, therapeutic responses to IL-17/IL-23 suppression are often limited, indicating significant immunological heterogeneity. There is growing evidence that type 2-associated immunological pathways may have a role in the persistence of disease in some patients. Herein, we report a 40-year-old woman with refractory PPP who had no personal or familial history of psoriasis or atopy. She was treated with stapokibart, an IL-4Rα monoclonal antibody that inhibits IL-4/IL-13 signaling, and experienced a rapid and long-lasting remission. Previous treatments, such as topical corticosteroids, retinoids, and Tripterygium wilfordii, were ineffective. Lesional skin exhibited moderate phosphorylated STAT6 positivity in scattered inflammatory infiltrates, independent of CD4+ T-cell presence, indicating engagement of canonical IL-4/IL-13 signaling at the tissue level, despite normal serum IgE levels and the lack of peripheral or tissue eosinophilia. The context-dependent clinical significance of Th2 pathway regulation in PPP is highlighted by a systematic literature review combined with our case. In non-atopic individuals, who frequently have noticeable pruritus despite unimpressive systemic atopic indicators, blockade of IL-4/IL-13 signaling has resulted in significant clinical relief. On the other hand, it has also been observed that blocking Th2-related pathways, such as IL-4/IL-13, IL-5, or IL-31, paradoxically causes PPP, highlighting the bidirectional and context-dependent significance of Th2 signaling in disease pathogenesis. Together with clinical characteristics like excessive pruritus, tissue-level Th2 activation may offer useful indicators to direct precision treatment in this diverse illness. - Source: PubMed
Publication date: 2026/08/13
Zhang YuqiHe YuexiLeng RaoLiu WeiZhou XiyuanYang Jianing - Suicide is an urgent public health crisis that claimed over 49,000 lives in the US in 2023. While genome-wide association studies of suicide are beginning to reveal genetic risk attributable to common variants with small effects on liability, these results explain only a fraction of the substantial proportion of risk due to genetics known to contribute to suicide mortality. As with other complex health conditions, some of this unexplained genetic risk is likely due to rarer variants with larger effects on liability. Using whole genome sequencing data from 1,054 population-ascertained suicide deaths from the Utah Suicide Mortality Research Study (USMRS) jointly processed with 1,230 controls, we investigated intragenic deletions as a class of genomic variation likely to disrupt gene function. To minimize false positives, deletions were limited to those found in large publicly available control datasets (1000 Genomes, GnomAD, and Centers for Common Disease Genomics) and where replication of deletions occurred across two cohorts within the USMRS suicides. Deletions meeting these filters were manually validated. Eleven deletions had at least 2-fold increase in frequency in suicide deaths vs. controls (range 2.28 to 4.46). Implicated genes were associated with mental health conditions (), epilepsy (), intellectual disability (), neuronal function (), metabolic function (), lipid metabolism (), immune functions (), and Alzheimer's disease (). Pending replication, these results may help prioritize biological pathways for future functional studies with the goal of increasing our understanding of risk mechanisms leading to suicide mortality. - Source: PubMed
Publication date: 2026/07/27
Coon HilaryDiBlasi EmilyNicholas ThomasMonson EricFerris ElliottShabalin AndreyYefimov LoganKeeshin BrooksBakian AmandaHan SeonggyunBaird LisaCallor WilliamStaley MichaelAmaro DierdreLi QingqinWillour Virginia - With six biologics available to treat severe asthma in 2025, choosing the optimal initial therapy and deciding to which other biologic to switch in case of insufficient benefit is challenging. To better understand patients' characteristics depending on the chosen biologic and patterns of switch, we evaluated adult patients with severe asthma from the GAN registry who were biologic-naïve at baseline. Between 2011 and 2024, 2,649 patients with severe asthma newly received a biologic, 26% anti-interleukin-5 receptor (IL5R), 25% anti-IL5, 16% anti-IL4R, 24% anti-immunoglobulin E (IgE), and 9% anti-thymic stromal lymphopoietin (TSLP). Distribution of biologics varied between time periods, reflecting their availability over time. Patients treated with anti-IgE were youngest at asthma diagnosis (mean 26 years) and had the highest rates of allergic comorbidities (80%). Blood eosinophils were highest in patients receiving anti-IL5R (median 433/µL) and lowest in those receiving anti-TSLP (median 159/µL), while FeNO was highest in patients treated with anti-IL5, anti-IL5R, or anti-IL4R (median 39, 38, and 35 ppb, respectively). 14.3% (n = 378) of patients were switched from the first biologic to a different one. The most frequent switch constellations were anti-IL5 to anti-IL5R, anti-IL5R to anti-IL4R, and anti-IL5 to anti-IL4R. After a switch, depending on the constellation up to 46% of patients reached remission. Phenotyping patients with severe asthma determines the choice of biologic therapy in real-world practice. Choice and switch of biologic have evolved over time influenced by availability of different drugs. Our analysis supports the practice of switching to a different biologic in case of insufficient initial response. - Source: PubMed
Publication date: 2026/07/20
Lenoir AlexandraBuhl RolandMuemmler CarloBehr JürgenEhmann RainerHamelmann EckardHoltdirk AnetteIdzko MarcoJandl MargretKaessner FrankSchmidt OlafSchulz ChristianSkowasch DirkSuhling HendrikTaube ChristianKorn StephanieMilger Katrin - Diabetic retinopathy (DR) reflects retinal microvascular injury and systemic immune-metabolic stress, and most public DR transcriptomic datasets lack paired microbiome/metabolomic profiles. We used gutMGene v2.0 as a curated microbe/metabolite-host gene prior and integrated it with peripheral blood transcriptomics from GSE221521. Candidate genes were refined by weighted gene co-expression network analysis (WGCNA), repeated resampling, cross-dataset assessment, mechanism scoring, peripheral blood mononuclear cell (PBMC) single-cell localization and filamin A ()-centered single-cell gene regulatory network (GRN) virtual knockout. The gutMGene prior contained 238 host genes; 15 DR-associated genes overlapped this prior, and WGCNA retained ten candidate gut microbe and microbial metabolite-related genes (GMMRGs): , , , , , , , , and . Resampling prioritized as the most consistent candidate. Cross-dataset assessment localized the strongest signal to type 2 diabetes (T2D) PBMCs, retinal endothelial cells and advanced proliferative diabetic retinopathy with diabetic macular edema (PDR + DME) retinal tissue, with weaker separation in whole blood, broad retinal tissue and six-donor type 1 diabetes (T1D) PBMCs. virtual knockout predicted cell-context-dependent perturbation of immune-related transcriptional programs, including in DR B cells and in DR monocytes/NK cells. This prior-guided study identifies within a ten-gene GMMRG set as a circulating host-response signal that links curated microbe/metabolite-host records to immune-vascular and cytoskeletal remodeling in DR. - Source: PubMed
Publication date: 2026/07/10
Ma ChuanxueWang YujunLiu Yi