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
- Air pollution-associated allergic airway inflammation is an increasing public health concern. Interleukin‑4 (IL‑4) and interleukin‑13 (IL‑13), which activate the Signal Transducer and Activator of Transcription 6 (STAT6) pathway, a central mediator of allergic airway inflammation, may modulate the respiratory toxicities of pollutants. The present study describes the generation and validation of a stable STAT6 luciferase reporter assay in human airway epithelial cells for evaluating environmental toxicants that modulate STAT6 signaling. Human bronchial epithelial 16HBE14o cells were transduced with a STAT6-responsive luciferase reporter using a lentiviral vector, followed by optimization of puromycin selection and multiplicity of infection, and monoclonal isolation by limiting dilution. A stable clone with strong and reproducible induction across serial passages was selected. Reporter responsiveness was validated by IL-4/IL-13 stimulation, and STAT6 dependence was confirmed using selective STAT6, STAT5, and STAT3 inhibitors. Assay performance was quantified by Z'-factor analysis, which indicated reproducible signal separation. Furthermore, the assay was applied to individual air-pollution constituents, and benzo[b]fluoranthene and particulate matter significantly increased STAT6 reporter activity. This method provides a scalable approach for measuring STAT6 activity in airway epithelial cells and for prioritizing environmental toxicants that modulate allergic airway signaling. - Source: PubMed
Publication date: 2026/08/25
Moonwiriyakit AekkachaPothipan PhattarinToyingsirikul DhanpisitSantiwong PawitLusawat Sirapop - IFNγ and IL-4, the canonical Th1 and Th2 cytokines, typically induce opposing macrophage polarization. Beyond their frequent coexistence and mutual antagonism in pathological settings, a synergistic crosstalk may also exist and remains to be defined. Through integrated transcriptomic, epigenomic, and CRISPR-based analyses, we identify that co-exposure to IL-4 and IFNγ results in an intermediate macrophage polarization state in murine macrophages, associated with a cohort of synergistically activated genes. We show that this synergistic activation is mediated by co-binding of STAT6 and STAT1 at regulatory regions marked with pronounced H3K27Ac accumulation and is dependent on the BRD4 cofactor. Deletion of either STAT factor or disruption of their binding motifs abolishes the synergistic transcriptional response. Our data support a model in which chromatin openness induced by one cytokine facilitates binding of the opposing cytokine-activated STAT transcription factor (TF), contributing to synergistic gene activation. We further show that IRF1, an IFNγ-induced TF whose expression persists in the presence of IL-4, is indispensable for a substantial subset of this program. Importantly, single-cell RNA sequencing of the PyMT murine breast cancer model reveals an in vivo tumor-associated macrophage subset showing STAT1 and STAT6 activation and is enriched for the synergistic gene signature. - Source: PubMed
Varga ZsófiaPoscher AnnaVáradi Eszter AnnaCinege GyöngyiIzsán AntalErdős EdinaBenyhe-Kis BernadettTihanyi Anna ZsuzsannaTzerpos PetrosBene KrisztiánHalász LászlóGémes NikolettNeuperger PatríciaTóth MártaMigh EdePóliska SzilárdSzebeni Gábor JWalter Jolán EDániel BenceCsörgő BálintNagy LászlóCzimmerer Zsolt - Calcitonin gene-related peptide (CGRP) is a key therapeutic target for migraine, yet its dual role in central neuroimmune regulation remains incompletely understood. This study reveals a critical paradox: while CGRP directly promotes anti-inflammatory activation of microglia in vitro, treatment with the CGRP receptor antagonist BIBN4096BS in a chronic migraine mouse model rapidly alleviated pain but was not accompanied by an increase in microglial anti-inflammatory markers, including CD206 and p-STAT6. This finding suggests that complete CGRP blockade may inadvertently attenuate a masked endogenous pro-repair tone. To supplement this signaling, we introduced IL-4 intervention. IL-4 not only restored microglial anti-inflammatory function via STAT6 pathway activation but also produced synergistic analgesic effects when combined with the CGRP antagonist, superior to either monotherapy. STAT6 overexpression further enhanced the anti-inflammatory effect of the CGRP and IL-4 combination, while STAT6 knockdown completely reversed this protective effect. These findings demonstrate that CGRP antagonism, while providing rapid analgesia, may come at the cost of suppressing neuroimmune repair. Combining CGRP antagonism with STAT6 pathway activation may offer a strategy to simultaneously block vasogenic pain and support immune homeostasis, providing a new conceptual framework for migraine therapy. - Source: PubMed
Publication date: 2026/08/25
Li ZichaoDan-Li Fan Zhen-ZhenCai Hong-BinGe Zhao-Ming - 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