Rat IL-4 ELISPOT kit, silver staining
- Known as:
- Rat Interleukin-4 ELISPOT reagent, silver staining
- Catalog number:
- ct081-t2
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- U-CyTech biosciences
- Gene target:
- Rat IL-4 ELISPOT kit silver staining
Related genes to: Rat 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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- Ulcerative colitis (UC), a chronic disease characterized by continuous damage to the intestinal mucosa and inflammation in the colon, comprises a series of gastrointestinal reactions and is difficult to cure. Here, we have designed a nanotherapeutic strategy combining pharmacotherapy with physical protection, which is achieved by constructing a green nanocarrier named cyclodextrin-based nanosponges (CDNSs) and encapsulating the insoluble drug parthenolide (PTL). CDNSs were transformed into a hydrogel driven by water, releasing the anti-inflammatory agent PTL and forming a sticky barrier in the position of the ulcer lesion to confront pathogenic bacteria at the same time. Notably, the resulting PTL-loaded CDNS (PTL@CDNS) had improved the solubility and intestinal cellular uptake of PTL. The orally delivered transformable PTL@CDNS via a colon-specific capsule significantly relieved UC in rats by enhancing the regulation of c-kit and STAT6 pathways as well as normalizing inflammatory cytokines, including IL-4, IL-6, IL-10, IL-13, nitric oxide, malondialdehyde, and TNF-α, with excellent biocompatibility. To sum up, transformable PTL@CDNSs were demonstrated as a promising strategy for in situ treatment of mucosal ulcers including UC. - Source: PubMed
Publication date: 2025/03/17
Guo JingwenHe YuanzhiLi JiaqiLin MinWu YihanYang JiayiHe ZehuiMeng LongWang ZhiXia QingZhu ChunyunZhang YongtaiFeng Nianping - Asthma is a chronic inflammatory disease characterized by dysregulated cytokine expression. The RNA-binding protein KSRP reduces the expression of several pro-inflammatory mediators. Therefore, we investigated whether KSRP modulates Th2-associated immune responses in vivo in an ovalbumin-induced (OVA) allergic asthma model in C57BL/6 KSRP-deficient mice (KSRP). - Source: PubMed
Publication date: 2025/03/17
Palzer Kim-AliciaBolduan VanessaLakus JelenaTubbe IngridMontermann EvelynClausen Björn EBros MatthiasPautz Andrea - Epidemiological evidence suggests that environmental pollutants precipitate the occurrence of allergic rhinitis (AR). The aryl hydrocarbon receptor (AhR), a receptor or sensor for various contaminants, is closely related to immunomodulation and the polarization of M2 macrophages. However, the mechanisms involving AhR and M2 macrophages in AR remain unclear. - Source: PubMed
Publication date: 2025/03/12
Liu QianDeng GuohaoJiang XianFu YanpengZhang JianWu XueLi XinlongAi JingangLiu HonghuiTan Guolin - Peritoneal dialysis (PD) can be used as renal replacement therapy when chronic kidney disease (CKD) progresses to end-stage renal disease. However, peritoneal fibrosis (PF) is a major cause of PD failure. Studies have demonstrated that PD fluid contains a significantly larger numbers of macrophages compared with the healthy individuals. During PD, macrophages can secrete cytokines to keep peritoneal tissue in sustained low-grade inflammation, and participate in the regulation of fibrosis-related signaling pathways, such as NF-κB, TGF-β/Smad, IL4/STAT6, and PI3K/AKT. A series of basic pathological changes occurs in peritoneal tissues, including epithelial mesenchymal transformation, overgeneration of neovasculature, and abnormal deposition of extracellular matrix. This review focuses on the role of macrophages in promoting PF during PD, summarizes the targets of macrophage-related inhibition of fibrosis, and provides new ideas for clinical research on delaying PF, maintaining the function and integrity of peritoneum, prolonging duration of PD as a renal replacement modality, and achieving longer survival in CKD patients. - Source: PubMed
Publication date: 2025/03/05
Chu ChenlingHuang YingCao LuxiJi ShuiyuZhu BinShen Quanquan - Disruption of local microbial irritation and host immune response can result in inflammation and tissue destruction in periodontitis. Studies on the modulation of macrophage polarization could help attenuate immune responses in periodontal tissues. To investigate the effect of ubiquitin-specific protease-7 (USP7) and its inhibitor P5091 on the polarization of macrophages in periodontitis, gene expression in periodontitis tissues and normal control were analyzed via single-cell RNA sequencing data and mice model experimental periodontitis. RAW264.7 cells were induced to M1 polarization with LPS + IFN-γ and M2 polarization with IL-4. USP7 was knocked down using lentivirus, and the effect of USP7 inhibitor P5091 on macrophage polarization was comparatively analyzed. The expression of Usp7 and polarization markers were detected by qRT-PCR. Western blot was used to examine the polarization markers and pathway-associated proteins. Results indicated that USP7 expression was elevated in tissues affected by periodontitis. Periodontitis macrophages and M1 polarized macrophages had higher USP7 expression. Knockdown of USP7 revealed an inhibition of both M1 and M2 macrophage polarization. Inhibition of USP7 with P5091 resulted in the decreased expression of M1 polarization markers and phosphorylation of P65, but the increased expression of M2 polarization markers and phosphorylation of STAT6. In conclusion, USP7 is involved in regulating macrophage polarization in periodontitis and its inhibitor P5091 may contribute to the prevention of periodontitis. - Source: PubMed
Publication date: 2025/02/12
Wang YanMu HailinYang BaochenYang ChangDong WeiWang Jiawei