Cymax Mouse IL-4 ELISA Kit
- Known as:
- Cymax Mouse Interleukin-4 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- lf-ek0268
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Abfrontier
- Gene target:
- Cymax Mouse IL-4 ELISA Kit
Related genes to: Cymax Mouse IL-4 ELISA Kit
- Gene:
- IL4 NIH gene
- Name:
- interleukin 4
- Previous symbol:
- -
- Synonyms:
- BSF1, IL-4, BCGF1, BCGF-1, MGC79402
- Chromosome:
- 5q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 1988-08-10
- Date modifiied:
- 2016-10-05
- Gene:
- TLR2 NIH gene
- Name:
- toll like receptor 2
- Previous symbol:
- -
- Synonyms:
- TIL4, CD282
- Chromosome:
- 4q31.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-06-25
- Date modifiied:
- 2016-10-25
Related products to: Cymax Mouse IL-4 ELISA Kit
Related articles to: Cymax Mouse IL-4 ELISA Kit
- This narrative review comprehensively elaborates the complicated interleukin (IL)-macrophage polarization axis as the core pathogenesis of allergic rhinitis (AR), focusing on layered molecular regulatory mechanisms covering inflammatory signaling, metabolic reprogramming and epigenetic modulation. Pro-inflammatory IL-1β, IL-6, IL-17 and TNF-α bind to TLR receptors to activate NF-κB, NLRP3 inflammasome and PI3K/Akt cascades, triggering M1 macrophage overactivation and acute nasal congestion, rhinorrhea via robust inflammatory mediator release. By contrast, anti-inflammatory IL-4 and IL-10 predominantly activate STAT6 signaling to drive abnormal M2 macrophage accumulation, sustaining persistent type 2 inflammation and irreversible nasal tissue remodeling; notably, IL-17 presents concentration-dependent bidirectional regulation on macrophage phenotypes. Metabolic reprogramming featured with glycolysis-oxidative phosphorylation switch, together with DNA methylation, histone modification and non-cRNA-mediated epigenetic regulation, serve as vital downstream executors linking IL signals to macrophage polarization imbalance. Conventional glucocorticoids, antihistamines and monoclonal antibodies including omalizumab and dupilumab (targeting IL-4Rα) exert therapeutic efficacy via intervening this axis, while multiple natural herbal constituents and classic TCM formulas also modulate relevant inflammatory pathways to alleviate AR symptoms. For translational application, the CD206/CD86 macrophage polarization ratio is highlighted as a representative candidate biomarker for disease severity assessment. Collectively, this review integrates multi-layered regulatory evidence and lays theoretical support for developing novel precision-targeted anti-allergic therapies. - Source: PubMed
Publication date: 2026/08/13
Peng WanyingXie LiangzhenLiu YuanchunLi Yan - Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by keratinocyte hyperproliferation, altered differentiation, barrier dysfunction, and oxidative stress. Currently available therapies, including monoclonal antibodies and JAK inhibitors, have improved AD management but do not address all aspects of the disease, supporting the investigation of natural-product strategies as complementary approaches to long-term care. An acute in vitro model of canine atopic-like inflammation was established by exposing canine progenitor epidermal keratinocytes (CPEK) for 24 h to a defined cytokine cocktail (IFN-γ, IL-4, IL-13), followed by 24 h of treatment with hemp oil, blackcurrant seed oil, vitamin D, or their combination. Proliferation (Ki-67, cell-cycle), differentiation (KRT5, KRT10, TGM1, involucrin), tight-junction organization (CLDN1, TJP1, ZO-1, TEER), wound closure, nitrosative stress (3-nitrotyrosine), the NRF2/BACH1/HMOX1 axis, and the secretion of STAT1- and NF-κB-dependent inflammatory mediators (CXCL9, CXCL10, IL-8, IL-6) and the STAT6-targeted chemokine CCL17 were assessed. The cytokine cocktail induced a coherent AD-like phenotype: increased Ki-67, downregulated CLDN1, sustained nitrosative stress, NRF2 elevation paralleled by BACH1 induction, and robust secretion of STAT1- and NF-κB-dependent mediators. The four treatments modulated this phenotype according to clearly differential, pathway-specific profiles. Vitamin D, alone or combined, emerged as the most effective modulator of proliferation and acted preferentially on the downstream redox arm, inducing HMOX1 and reducing BACH1; both vitamin D-containing formulations exerted broad anti-inflammatory activity across the STAT1 and NF-κB axes. Hemp oil acted preferentially on tight-junction integrity (CLDN1 recovery), on the upstream NRF2 arm (NFE2L2 induction), on the STAT1 chemokine arm (CXCL9, CXCL10 reduction), and on wound closure. Blackcurrant seed oil acted preferentially on NF-κB-dependent IL-8 and on early wound-closure dynamics. This differential pharmacological footprint provides a rational basis for further investigation of these formulations as nutraceutical adjuncts in canine AD. - Source: PubMed
Tortolani DanielScipioni LuciaAnselmucci AlessandroCiaramellano FrancescaDi Leonardo MeriFusaro IsaOddi SergioGramenzi Alessandro - Signal Transducer and Activator of Transcription 6 (STAT6) is a critical transcription factor in the interleukin-4 (IL-4) and IL-13 signaling pathways and serves as a key pathogenic driver of type 2 (TH2) immune responses. Dysregulated STAT6 activity is implicated in asthma, atopic dermatitis, autoimmune diseases, eosinophilic disorders, and certain cancers. As such, targeting STAT6 presents a promising therapeutic strategy for these diseases. - Source: PubMed
Publication date: 2026/08/07
Khan Muhammad Zafar IrshadDu Bo-QunXue MeiYu Meng-QianLi Shun-RanWang JiansheWang Chen-ChenYe Xiang-Yang - To observe the effect of electroacupuncture(EA) intervention on the interleukin-4 (IL-4)/Janus kinase 1 (JAK1)/signal transducer and activator of transcription 6 (STAT6) signaling pathway in colon tissue of chronic ulcerative colitis (UC) mouse model, in order to explore the potential mechanism of EA in promoting M2 macrophage polarization and improving intestinal mucosal barrier injury in UC mice. - Source: PubMed
Hu Xiao-MeiZhang HongTang Ya-SiPan Yan-YingZhuo YueDeng Shi-FengYi Xi-Qin - Bitter taste receptors are distributed in various non-taste tissues and cells, where they exert crucial roles in neuroimmune regulation and inflammatory response. In this study, a mouse model of fine particle (FPs) exposure was established by nebulized ovalbumin (OVA) inhalation to investigate the effects of FPs on renal function and structure. The experiment results revealed that inhalation of OVA led to glomerular atrophy, and renal tubular epithelial cell swelling and vacuolization, accompanied by increased levels of blood urea nitrogen and creatinine in the bloodstream. OVA inhalation induced a significant elevation in the levels of HO and malondialdehyde (MDA), while significantly decreased the activity of total superoxide dismutase (T-SOD) and the content of glutathione (GSH) in renal tissues. Furthermore, OVA downregulated Th1 cytokine IFN-γ, upregulated Th2 cytokines IL-4, IL-5 and IL-13, and activated pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) as well as genes involved in inflammatory pathways (TLR-2, TLR-4, MyD88, NF-κB, JAK-1, JAK-2, JAK-3, STAT-3, STAT-6). Notably, OVA-induced kidney injury was accompanied by the downregulation of bitter taste receptors and their downstream signaling molecules (α-gustducin, transient receptor potential melastatin 5 [Trpm5]). However, gavage administration of multi-strain probiotics significantly alleviated the toxic effects of OVA on the mouse kidneys, as evidenced by the reversal of the aforementioned abnormal changes in renal structure, biochemical indicators, oxidative stress markers, inflammatory factors, and bitter taste transduction-related molecules. Collectively, these findings indicate that OVA-induced distal organ injury, particularly renal injury, is associated with systemic inflammation and the inhibition of bitter taste transduction pathways. The protective effect of multi-strain probiotics on OVA-inhaled mice is correlated with the activation of bitter taste transduction, as well as the regulation of immune balance and inflammatory responses. - Source: PubMed
Publication date: 2026/07/22
Jiao SiweiZhang RuigangPei YaochenWang MuhuaMa JiePeng XiaoguangYi Huilan