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
- 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 - Integration of intracellular signalling and metabolic reprogramming is critical for macrophage polarisation and the induction of pro- or anti-inflammatory responses. However, the molecular switches that govern these processes remain incompletely defined. While 4-1BB ligand (4-1BBL), a member of the TNF superfamily, is known to promote sustained pro-inflammatory responses in macrophages, its role in anti-inflammatory macrophage responses has not been fully elucidated. This study identifies that 4-1BBL serves as a negative regulator of anti-inflammatory macrophage polarisation. Genetic deletion or pharmacological inhibition of 4-1BBL significantly enhanced the expression of anti-inflammatory cytokines and markers in mouse macrophages. In IL-4R signalling, 4-1BBL restrained Janus kinase 1 (JAK1) and signal transducer and activator of transcription 6 (STAT6) phosphorylation, thereby modulating transcriptional programmes associated with anti-inflammatory macrophage activation. Consistently, 4-1BBL deficiency elevated mitochondrial oxidative phosphorylation and fatty acid oxidation, accompanied by increased expression of metabolic genes in anti-inflammatory macrophages. Transcriptomic analysis further revealed a shift towards anti-inflammatory and oxidative metabolic gene signatures in IL-4-treated 4-1BBL-deficient macrophages. Importantly, the inhibition of 4-1BBL signalling also augmented anti-inflammatory responses in human monocytes and facilitated the transition from pro-inflammatory to anti-inflammatory phenotypes. Collectively, these findings establish 4-1BBL as a crucial molecular switch that regulates macrophage polarisation by integrating inflammatory signalling with metabolic reprogramming, highlighting 4-1BBL as a potential therapeutic target for promoting inflammation resolution. - Source: PubMed
Publication date: 2026/07/27
Kang Young Jun - Allergen immunotherapy (AIT) remains the only disease-modifying treatment for immunoglobulin (Ig) E-mediated allergic diseases, including allergic rhinitis (AR), asthma, food allergy, and atopic dermatitis (AD). This review provides a comprehensive update on recent advances in AIT, focusing on immunological mechanisms, novel vaccines, biomarkers, clinical outcomes across different diseases, and emerging combination strategies with biologics. We discussed the pivotal roles of regulatory T and B cells, innate lymphoid cells (ILCs), and blocking antibodies (immunoglobulin G4 [IgG4], immunoglobulin A [IgA]) in establishing long-term tolerance. Novel allergen vaccines-including recombinant and hypoallergenic derivatives, virus-like particle (VLP) conjugates, and transgenic peptide vaccines-aim to improve safety and efficacy. We critically evaluate current biomarkers for predicting and monitoring AIT response, such as the allergen-specific IgE (sIgE)/total immunoglobulin E (tIgE) ratio, basophil activation test, and cellular markers. Clinical evidence supports AIT efficacy in asthma, AR, and AD, with emerging applications in food allergies. Furthermore, combining AIT with biologics (e.g., anti-IgE and anti-interleukin [IL]-4/IL-4 receptor [IL-4R]) shows promise in enhancing safety and efficacy, particularly in severe asthma. Despite these advances, challenges remain in patient selection, treatment duration, and extract standardization. Future research should prioritize predictive biomarkers, short-course regimens, and synergistic biologic-AIT approaches. - Source: PubMed
Publication date: 2026/07/23
Fu WeiZheng YangChen HaoDong XiangLi WeiLiang HuilingChen ShiweiAkdis Cezmi AGao Yadong - : Severe asthma and chronic rhinosinusitis with nasal polyps (CRSwNP) frequently coexist and are associated with type 2 inflammation, leading to poor symptom control and high healthcare burden. Biologic therapies targeting IL-4Rα and IL-5/IL-5R have shown efficacy in type 2 inflammatory asthma and CRSwNP, but comprehensive evidence on their efficacy, safety, and research trends is limited. : We conducted a systematic review and meta-analysis of randomized controlled trials (RCTs) evaluating dupilumab, mepolizumab, benralizumab, or reslizumab in patients with type 2 inflammatory asthma and/or CRSwNP. Primary outcomes included lung function (FEV1), symptom control (ACQ, SNOT-22, nasal polyp score), and serious adverse events (SAEs). Risk of bias was assessed using the Cochrane RoB 2.0 tool. Publication bias was evaluated with funnel plots and Trim-and-Fill analysis. Bibliometric analysis was performed to identify publication trends and emerging research directions. : A total of 23 RCTs involving 8758 participants were included. Biologic therapy was not associated with a significant increase in serious adverse events (RR = 1.15, 95% CI: 0.89-1.50). Compared with control treatment, biologics significantly improved FEV1 (MD = 100.67 mL, 95% CI: 65.94-135.40) and ACQ scores (MD = -0.40, 95% CI: -0.54 to -0.25). In patients with CRSwNP and comorbid asthma, biologics also improved SNOT-22 scores (MD = -13.16, 95% CI: -24.85 to -1.47) and nasal polyp scores (MD = -1.31, 95% CI: -1.95 to -0.68). Dupilumab trials showed larger reductions in nasal polyp score than IL-5/IL-5R-targeted trials, although this indirect comparison should be interpreted cautiously. Bibliometric analysis indicated increasing research attention to upstream epithelial targets such as TSLP. : Both IL-4Rα and IL-5/IL-5R-targeted biologics are effective and well-tolerated in type 2 inflammatory airway diseases. IL-4Rα inhibition shows favorable upper-airway outcomes in CRSwNP with asthma, but head-to-head trials are needed to clarify its comparative efficacy relative to IL-5/IL-5R-targeted therapies. Emerging research directions are shifting toward upstream epithelial alarmin antibodies. - Source: PubMed
Publication date: 2026/06/26
Li ZhuojunJiang MaoyuChen MaiqiLiu Yehai