Rat IL-4 ELISPOT kit, enzymatic staining
- Known as:
- Rat Interleukin-4 ELISPOT reagent, enzymatic staining
- Catalog number:
- ct081-pr2
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- U-CyTech biosciences
- Gene target:
- Rat IL-4 ELISPOT kit enzymatic staining
Related genes to: Rat IL-4 ELISPOT kit, enzymatic 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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- 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 - Limited therapeutic options are available for patients with advanced-stage mycosis fungoides (MF), and the 5-year survival rate is 25%. Due to its critical role in MF pathogenesis, the IL4/IL13 pathway presents a promising target for treatment. Here, we analyzed blocking of IL4Rα, the common subunit of the IL4 and IL13 receptors, within the advanced-stage MF cutaneous tumor microenvironment (TME). - Source: PubMed
Publication date: 2026/06/25
Gaydosik Alyxzandria MWang AlysonDas JishnuLapolla BrigitAkilov Oleg EGeskin Larisa JFuschiotti Patrizia - Atopic dermatitis (AD) is a chronic immune-mediated inflammatory skin disease characterized by a complex and dynamic interplay between immune dysregulation and epidermal barrier dysfunction. Emerging evidence supports an integrated pathogenic model in which immune activation and barrier impairment form a bidirectional and self-reinforcing axis rather than representing separate processes. This review synthesizes current knowledge on the role of IL-4/IL-13-dependent signaling in regulating keratinocyte lipid metabolism and its impact on epidermal barrier integrity. IL-4/IL-13 signaling via the JAK-STAT pathway, particularly STAT6, contributes to keratinocyte dysfunction, resulting in impaired differentiation and coordinated alterations in lipid metabolism, including fatty acid elongation and ceramide synthesis. These cytokine-driven processes disrupt the organization of the stratum corneum lipid matrix, resulting in increased transepidermal water loss, enhanced skin permeability, and susceptibility to microbial colonization, thereby promoting chronic inflammation. Collectively, these findings support the concept that IL-4/IL-13-mediated dysregulation of keratinocyte lipid metabolism may represent an important immunometabolic mechanism linking type 2 inflammation with secondary barrier dysfunction in atopic dermatitis, thereby contributing to disease persistence. Targeting both immune pathways and epidermal lipid homeostasis may represent an effective strategy to restore barrier function and improve clinical outcomes. - Source: PubMed
Publication date: 2026/06/22
Andrzejczak KlaraSternak AgataWitkowski WiktorFlak AleksandraMaj JoannaPonikowska Małgorzata