Monkey IL-4 ELISPOT kit, silver staining
- Known as:
- Monkey Interleukin-4 ELISPOT reagent, silver staining
- Catalog number:
- ct128-pb5
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- U-CyTech biosciences
- Gene target:
- Monkey IL-4 ELISPOT kit silver staining
Related genes to: Monkey IL-4 ELISPOT kit, silver staining
- 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
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- 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 - ABCB5+ dermal mesenchymal stem cells (DMSCs) regulate macrophage activation via interleukin-1 receptor antagonist (IL-1Ra), but upstream control mechanisms remain unclear. Here, we define a dual-signal model integrating inflammatory and type 2 cytokine pathways. IFNγ/LPS priming initiates IL-1Ra expression, while IL-4 signaling through IL-4Rα amplifies this response via STAT6 in both ABCB5+ DMSCs and macrophages. In coculture, ABCB5+ DMSCs drive macrophage polarization toward a CD206+/CD163+ phenotype with enrichment of CD163-expressing subsets. IL-4Rα blockade with dupilumab inhibits STAT6 activation, suppresses IL-1Ra amplification, and attenuates expansion of this IL-4Rα-dependent macrophage population. Collectively, these findings identify IL-4/IL-4Rα/STAT6 signaling as a conserved amplifier of IL-1Ra-mediated stromal-immune crosstalk. - Source: PubMed
Publication date: 2026/07/08
Singh KarmveerWilson Brian JWaaga-Gasser Ana MariaSchatz SusanneHainzl AdelheidYeung Philip CMaity PallabFrank Natasha YScharffetter-Kochanek KarinFrank Markus H - Chronic psychological stress promotes cancer progression by activating tumor-associated macrophages (TAMs), particularly through polarization toward the pro-tumorigenic M2 phenotype. However, therapeutic strategies targeting stress-induced macrophage polarization remain limited. This study investigated whether the ethanolic extract of Bupleurum falcatum L. root (EBF) can modulate chronic stress-driven TAM polarization. To simulate a stress-associated microenvironment, norepinephrine (NE) was used to treat 4 T1 breast cancer cells. Conditioned media from NE-treated cells (NE CM) significantly upregulated M2 macrophage markers and STAT6 phosphorylation in RAW 264.7 cells; however, these effects were markedly attenuated by EBF. Consequently, EBF inhibited M2 macrophage-induced cancer cell migration. Notably, EBF treatment modulated the tumor cell secretome, as CM from 4 T1 cells co-treated with NE and EBF failed to induce M2 polarization. Network pharmacology analysis identified interleukin (IL)-4 as a key mediator-upregulated by NE and suppressed by EBF-among the overlapping genes shared by cancer metastasis, BF, and M2 macrophage-associated gene sets. Furthermore, saikosaponins A, C, and D consistently contributed to these regulatory effects. Collectively, our findings demonstrate that EBF inhibits NE-driven M2 polarization and subsequent macrophage-mediated cancer progression, suggesting its potential as a therapeutic agent to modulate the tumor microenvironment under chronic stress conditions. - Source: PubMed
Publication date: 2026/07/06
Jeong Jae-HoonPark Shin-Hyung - Giant papillae formation along with corneal damage in vernal keratoconjunctivitis (VKC) is primarily mediated by type 2 inflammation and eosinophils. Corneal keratocytes are the primary cellular source of eotaxin at the ocular surface, facilitating eosinophil migration to the cornea. We aimed to elucidate the role of the transcription factor signal transducer and activator of transcription 6 (STAT6) in eotaxin expression by corneal fibroblasts and to evaluate the inhibitory effects of rebamipide-a mucin secretagogue with reported therapeutic potential in VKC-on this pathway. Human corneal fibroblasts were cultured and stimulated with interleukin (IL)-4 or IL-13, and subsequently preincubated with either a STAT6 inhibitor (AS1517499) or rebamipide prior to cytokine stimulation. STAT6 phosphorylation was evaluated by Western blotting. Eotaxin expression was assessed using an enzyme-linked immunosorbent assay and a real-time polymerase chain reaction. IL-4 and IL-13 stimulation induced STAT6 phosphorylation and increased eotaxin production at mRNA and protein levels. Preincubation with both AS1517499 and rebamipide suppressed IL-4- or IL-13-induced STAT6 phosphorylation, significantly reducing eotaxin mRNA and protein expression. These findings demonstrate that IL-4- or IL-13-stimulated eotaxin production in human corneal fibroblasts is mediated through the STAT6 signaling pathway. Rebamipide inhibited STAT6 activation, leading to reduced eotaxin production, suggesting that its therapeutic effect in VKC is due to the suppression of STAT6-mediated eotaxin production, which may reduce eosinophil accumulation to the cornea. - Source: PubMed
Publication date: 2026/06/27
Sakaguchi HidetoFukuda KenIshida WakaMoribe Juliana HiroyoNakajima IsanaKishimoto TatsumaYamashiro Kenji