人 IL25 抗体对
01AB03552
Interleukin 25 (IL25), also known as IL-17E, is a member of the IL-17 cytokine family that plays a pivotal role in driving type 2 immunity. It signals through a heterohexameric receptor complex consisting of IL-17RB and IL-17RA, which activates downstream pathways including NF-κB, MAPK, and JAK2-STAT5. This signaling cascade promotes the production of Th2 cytokines such as IL-4, IL-5, and IL-13, while simultaneously inhibiting Th17 cell differentiation. Produced by epithelial cells, tuft cells, and various immune cells, IL-25 is a key initiator of allergic and anti-helminthic responses. Clinically, IL-25 is well-established as a mediator of allergic asthma, where it contributes to airway remodeling and eosinophilic inflammation. It is also implicated in inflammatory bowel disease through the dysregulation of the tuft cell-ILC2 axis, although it can also exhibit context-dependent protective effects on intestinal barrier integrity.
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技术参数
- 靶点基因名
- IL25
- 基因别名
- IL17E
- 蛋白别名
- interleukin 25; IL25
- UniProt
- Q9H293
- 物种
- Human
产品详情
- 靶点名称
- IL25
- 蛋白名称
- interleukin 25
- 蛋白别名
- Interleukin-25; IL-25; Interleukin-17E; IL-17E
- 靶点基因名
- IL25
- 基因别名
- IL17E
- UniProt
- Q9H293
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
Interleukin 25 (IL25), also known as IL-17E, is a member of the IL-17 cytokine family that plays a pivotal role in driving type 2 immunity. It signals through a heterohexameric receptor complex consisting of IL-17RB and IL-17RA, which activates downstream pathways including NF-κB, MAPK, and JAK2-STAT5. This signaling cascade promotes the production of Th2 cytokines such as IL-4, IL-5, and IL-13, while simultaneously inhibiting Th17 cell differentiation. Produced by epithelial cells, tuft cells, and various immune cells, IL-25 is a key initiator of allergic and anti-helminthic responses. Clinically, IL-25 is well-established as a mediator of allergic asthma, where it contributes to airway remodeling and eosinophilic inflammation. It is also implicated in inflammatory bowel disease through the dysregulation of the tuft cell-ILC2 axis, although it can also exhibit context-dependent protective effects on intestinal barrier integrity.