抗人 IL17D 抗体对
01AB03542
Interleukin 17D (IL17D) is a secreted pro-inflammatory cytokine and a member of the IL-17 family, primarily expressed in skeletal muscle, heart, adipose tissue, and the nervous system. As a disulfide-linked homodimer, it modulates immune responses by stimulating the production of myeloid growth factors and chemokines, such as IL-6, IL-8, and GM-CSF, from endothelial cells and other target tissues. This signaling is mediated through the activation of the nuclear factor kappa-B pathway. During acute infection, IL-17D can exert pathogenic effects by suppressing CD8+ T cell activity and dendritic cell function, thereby impairing adaptive immunity. Clinically, dysregulated IL-17D expression is associated with chronic inflammatory conditions, including psoriasis and hidradenitis suppurativa. Furthermore, it has been implicated in lung cancer progression by promoting tumor-associated macrophage infiltration via p38 MAPK signaling.
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技术参数
- 靶点基因名
- IL17D
- 蛋白别名
- interleukin 17D; IL17D
- UniProt
- Q8TAD2
- 物种
- Human
产品详情
- 靶点名称
- IL17D
- 蛋白名称
- interleukin 17D
- 蛋白别名
- Interleukin-17D; IL-17D; Interleukin-27; IL-27
- 靶点基因名
- IL17D
- UniProt
- Q8TAD2
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
Interleukin 17D (IL17D) is a secreted pro-inflammatory cytokine and a member of the IL-17 family, primarily expressed in skeletal muscle, heart, adipose tissue, and the nervous system. As a disulfide-linked homodimer, it modulates immune responses by stimulating the production of myeloid growth factors and chemokines, such as IL-6, IL-8, and GM-CSF, from endothelial cells and other target tissues. This signaling is mediated through the activation of the nuclear factor kappa-B pathway. During acute infection, IL-17D can exert pathogenic effects by suppressing CD8+ T cell activity and dendritic cell function, thereby impairing adaptive immunity. Clinically, dysregulated IL-17D expression is associated with chronic inflammatory conditions, including psoriasis and hidradenitis suppurativa. Furthermore, it has been implicated in lung cancer progression by promoting tumor-associated macrophage infiltration via p38 MAPK signaling.