IL25 Protein
- Known as:
- IL25 Protein
- Catalog number:
- 10096-H01H
- Product Quantity:
- 50
- Category:
- -
- Supplier:
- Smart Serology
- Gene target:
- IL25 Protein
Related genes to: IL25 Protein
- Gene:
- IL25 NIH gene
- Name:
- interleukin 25
- Previous symbol:
- IL17E
- Synonyms:
- IL-25, IL-17E
- Chromosome:
- 14q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-01-26
- Date modifiied:
- 2014-11-19
- Gene:
- MYDGF NIH gene
- Name:
- myeloid derived growth factor
- Previous symbol:
- IL27, IL27w, C19orf10
- Synonyms:
- R33729_1, IL25, SF20, IL-25, IL-27
- Chromosome:
- 19p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2002-04-03
- Date modifiied:
- 2016-11-16
Related products to: IL25 Protein
Related articles to: IL25 Protein
- Liver Fibrosis (LFib) represents a significant global health burden as a chronic progressive disease. Emerging evidence has established a critical link between macrophage extracellular traps (METs) and LFib; however, the precise triggers of METs formation and their mechanistic contributions to fibrosis remain poorly understood. Substantial evidence indicates that interleukin-25 (IL-25) potently regulates macrophage metabolism and LFib progression. A carbon tetrachloride (CCl₄)-induced mouse model of liver fibrosis spanning distinct stages (2 to 8 weeks) was established. In vitro studies utilized co-culture systems and conditioned medium treatment to assess METs-mediated activation of hepatic stellate cells (HSCs). To elucidate the specific role of IL-25, hepatocyte-specific IL-25 conditional knockout (IL-25CKO) mice were generated using CRISPR/Cas9 technology and subjected to the LFib model. Mechanistic investigations involved stimulating RAW 264.7 macrophages with rmIl-25 and specific inhibitors. Techniques such as scanning/transmission electron microscopy, immunofluorescence, Western blot and ELISA were employed to analyze MET formation, ROS production, lysosomal activation, mitophagy, and related signaling pathways. Fibrotic livers exhibited strong early co-localization of IL-25 with hepatocytes, which preceded METs formation. This demonstrates that early production of IL-25 by hepatocytes acts as a triggering factor for METs formation. In vitro co-culture systems revealed METs-mediated activation of HSCs, while mechanistic studies showed that IL-25 promotes IL-17RB receptor activation, triggering downstream reactive oxygen species (ROS) bursts, lysosomal activation, and METs formation. This work identifies a pathogenic hepatocyte-macrophage-HSC axis and supports IL-25 early blockade as a promising clinical strategy for LFib. - Source: PubMed
Publication date: 2026/04/01
Cao Cheng-JiangYang MingDu Chang-LinFang XueSong He-HangWang Wen-JingWang Miao-MiaoZhang Wen-MeiLiu Zhen-LongHuang ChengLi Jun - Small intestinal (SI) tuft cells are critical sentinels for innate type 2 immunity against helminths, but their role in adaptive responses is unclear. We show that despite the presence of protective memory CD4 T helper 2 (Th2) cells, tuft cells remain essential for worm clearance during a secondary infection with Heligmosomoides polygyrus bakeri (H. polygyrus bakeri). Th2 cells still develop in the absence of tuft cells or group 2 innate lymphoid cells but upregulate receptors for tuft cell effectors interleukin-25 (IL-25) and leukotriene C (LTC) when they enter the SI. IL-25 and LTC are sufficient to drive IL-13 production by Th2 cells, and their absence during a secondary infection diminishes IL-13. Complete restriction of a secondary H. polygyrus bakeri infection requires granulomas that reduce worm fitness together with tuft cell-dependent clearance from the intestinal lumen. Thus, tuft cells regulate both innate and adaptive immunity, and we extend the paradigm that Th2 cells require tissue-specific cues for optimal function. - Source: PubMed
Publication date: 2026/03/27
Stanbery Alison GBillipp Tyler EWebeck Lily MRubio Brianna RamirezNadjsombati Marija SBell Madeleine RMcGinty John WPepper MarionMoltke Jakob von - is a zoonotic pathogen capable of invading the host through the intestinal mucosa. However, the immune mechanisms underlying intestinal infection remain poorly understood. Tuft cells are specialized chemosensory epithelial cells in the intestine that can detect pathogen invasion and secrete IL-25, subsequently activating type 2 innate lymphoid cells (ILC2s) and playing a critical role in anti-parasitic immune responses. Nevertheless, whether the tuft cell-ILC2 circuit participates in immune responses against bacterial infections remains unclear. This study aimed to investigate the dynamic changes of tuft cells and ILC2s following infection, with a particular focus on elucidating the regulatory role of IL-25 in this process. - Source: PubMed
Publication date: 2026/02/06
Shang KaiyuChen NaTian TingtingShi HuidongShi JuanQi XinxinZhu YuejieZhang Fengbo - Traumatic brain injury (TBI) causes severe disruption of the blood-brain barrier (BBB), a key event that contributes to secondary neurological damage. Interleukin-25 (IL-25) has recently emerged as an important regulator of neuroinflammation, yet its role in BBB repair after TBI remains unclear. This study investigated the protective effects of IL-25 on BBB integrity and neurological function in mice following TBI and explored the underlying mechanisms. - Source: PubMed
Publication date: 2026/01/12
Peng MinShu DaoxingChen ZhengYang ZhijieZhang MaosongWang QifuShao Xuefei - Hepatic steatosis is characterised by hepatic lipid accumulation, inflammation and fibrosis, with macrophage polarisation playing a central role in disease progression. This study investigates the role of interleukin-25 (IL-25) in modulating macrophage polarisation and Notch signalling in a methionine-choline-deficient (MCD) diet-induced metabolic dysfunction-associated fatty liver disease (MAFLD) model. - Source: PubMed
Zheng XuelianHu DandanZhang DongjingChen YeWei JianruiXie BoWang Anjiang