Recombinant Human IL-4
- Known as:
- Recombinant Human Interleukin-4
- Catalog number:
- sjb02-03
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Amoy diagnostics
- Gene target:
- Recombinant Human IL-4
Related genes to: Recombinant Human IL-4
- 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: Recombinant Human IL-4
Related articles to: Recombinant Human IL-4
- Allergic inflammation, which is the pathogenesis of allergic rhinitis and asthma, is associated with disruption of the airway epithelial barrier due to the effects of type 2 inflammatory cytokines, i.e. interleukin-4 and interleukin-13 (IL-4/13). The anti-allergic inflammatory effect of β-eudesmol (BE) on the tight junction (TJ) of the airway epithelium has not previously been reported. Herein, the barrier protective effect of BE was determined by measurement of transepithelial electrical resistance and by paracellular permeability assay in an IL-4/13-treated 16HBE14o- monolayer. Pre-treatment of BE concentration- and time- dependently inhibited IL-4/13-induced TJ barrier disruption, with the most significant effect observed at 20 μM. Cytotoxicity analyses showed that BE, either alone or in combination with IL-4/13, had no effect on cell viability. Western blot and immunofluorescence analyses showed that BE inhibited IL-4/13-induced mislocalization of TJ components, including occludin and zonula occludens-1 (ZO-1), without affecting the expression of these two proteins. In addition, the mechanism of the TJ-protective effect of BE was mediated by inhibition of IL-4/13-induced STAT6 phosphorylation, in which BE might serve as an antagonist of cytokine receptors. In silico molecular docking analysis demonstrated that BE potentially interacted with the site I pocket of the type 2 IL-4 receptor, likely at Asn-126 and Tyr-127 amino acid residues. It can therefore be concluded that BE is able to prevent IL-4/13-induced TJ disassembly by interfering with cytokine-receptor interaction, leading to suppression of STAT6-induced mislocalization of occludin and ZO-1. BE is a promising candidate for a therapeutic intervention for inflammatory airway epithelial disorders driven by IL-4/13. - Source: PubMed
Publication date: 2024/04/30
Tharabenjasin PhuntilaMoonwiriyakit AekkachaSontikun JenjiraTimpratueang KanokphornKuno SuhaibeeAiebchun ThitinanJongkon NathjananMongkolrob RungraweePabalan NoelChoowongkomon KiattaweeMuanprasat Chatchai - Iguratimod is a novel synthetic, small-molecule immunosuppressive agent used to treat rheumatoid arthritis. Through ongoing exploration of its role and mechanisms of action, iguratimod has been observed to have antifibrotic effects in the lung and skin; however, its effect on renal fibrosis remains unknown. This study aimed to investigate whether iguratimod could affect renal fibrosis progression. Three different concentrations of iguratimod (30 mg/kg/day, 10 mg/kg/day, and 3 mg/kg/day) were used to intervene in unilateral ureteral obstruction (UUO) model mice. Iguratimod at 10 mg/kg/day was observed to be effective in slowing UUO-mediated renal fibrosis. In addition, stimulating bone marrow-derived macrophages with IL-4 and/or iguratimod, or with TGF-β and iguratimod or SRC inhibitors , suggested that iguratimod mitigates the progression of renal fibrosis in UUO mice, at least in part, by inhibiting the IL-4/STAT6 signaling pathway to attenuate renal M2 macrophage infiltration, as well as by impeding SRC activation to reduce macrophage-myofibroblast transition. These findings reveal the potential of iguratimod as a treatment for renal disease. - Source: PubMed
Publication date: 2024/04/26
Zhou YueyuanLi ZhilanYu ShenyiWang XuanXie TingtingZhang Weiru - Macrophages are critical to turn noninflamed "cold tumors" into inflamed "hot tumors". Emerging evidence indicates abnormal cholesterol metabolites in the tumor microenvironment (TME) with unclear function. Here, we uncovered the inducible expression of cholesterol-25-hydroxylase (Ch25h) by interleukin-4 (IL-4) and interleukin-13 (IL-13) via the transcription factor STAT6, causing 25-hydroxycholesterol (25HC) accumulation. scRNA-seq analysis confirmed that CH25H subsets were enriched in immunosuppressive macrophage subsets and correlated to lower survival rates in pan-cancers. Targeting CH25H abrogated macrophage immunosuppressive function to enhance infiltrating T cell numbers and activation, which synergized with anti-PD-1 to improve anti-tumor efficacy. Mechanically, lysosome-accumulated 25HC competed with cholesterol for GPR155 binding to inhibit the kinase mTORC1, leading to AMPKα activation and metabolic reprogramming. AMPKα also phosphorylated STAT6 Ser564 to enhance STAT6 activation and ARG1 production. Together, we propose CH25H as an immunometabolic checkpoint, which manipulates macrophage fate to reshape CD8 T cell surveillance and anti-tumor response. - Source: PubMed
Publication date: 2024/04/12
Xiao JunWang ShuangChen LonglongDing XinyuDang YuanhaoHan MingshunZheng YuxiaoShen HuanWu SifanWang MingchangYang DanLi NaDong ChenHu MiaoSu ChenLi WeiyunHui LijianYe YouqiongTang HuiruWei BinWang Hongyan - Regulatory CD4 T cells (Tregs) are pivotal for inhibition of autoimmunity. Primary sclerosing cholangitis (PSC) is an autoimmune cholestatic liver disease of unknown etiology where contribution of Tregs is still unclear. Activation of the JAK-STAT pathway critically modifies functions of Tregs. In PSC, we studied activation of STAT proteins and Treg functions in response to cytokines. - Source: PubMed
Dold LeonaKalthoff SandraFrank LeonieZhou TaotaoEsser PiaLutz PhilippStrassburg Christian PSpengler UlrichLanghans Bettina - Spinal cord injury (SCI) induces severe neuroinflammation, and subsequently neurological dysfunction. Activated microglia are critical for modulation of neuroinflammation. Protein tyrosine phosphatase receptor type O (PTPRO), a member of protein tyrosine phosphatases (PTPs), exerts a pro-inflammatory role in multiple human diseases; however, its role in SCI remains unclarified. Here, a T7 spinal cord compression injury model was established in Sprague-Dawley (SD) rats, and PTPRO expression was upregulated in injured spinal cord and microglia after SCI. Microglia M1 and M2 polarization in vitro were induced using LPS/IFN-γ and IL-4, respectively. PTPRO expression was elevated in M1-polarized microglia, and PTPRO downregulation mediated by PTPRO shRNA (shPTPRO) decreased CD86 cell proportion, iNOS, TNF-α, IL-1β, and IL-6 levels, and p65 phosphorylation. PTPRO was downregulated in M2 microglia, and PTPRO upregulation by PTPRO overexpression plasmid (OE-PTPRO) reduced CD206 cell percentage, Arg-1, IL-10, and TGF-β1 levels and STAT6 phosphorylation. Mechanistically, the transcription factor SOX4 elevated PTPRO expression and its promoter activity. SOX4 overexpression enhanced M1 polarization and p65 phosphorylation, while its knockdown promoted M2 polarization and STAT6 phosphorylation. PTPRO might mediate the function of SOX4 in BV2 microglia polarization. Furthermore, lentivirus-mediated downregulation of PTPRO following SCI improved locomotor functional recovery, demonstrated by elevated BBB scores, incline angle, consistent hindlimb coordination, and reduced lesion area and neuronal apoptosis. PTPRO downregulation promoted microglia M2 polarization, NF-κB inactivation and STAT6 activation after injury. In conclusion, PTPRO inhibition improves spinal cord injury through facilitating M2 microglia polarization via the NF-κB/STAT6 signaling pathway, which is probably controlled by SOX4. - Source: PubMed
Publication date: 2024/03/31
Zhang HaocongXiang LiangbiYuan HongYu Hailong