1. 重组蛋白
  2. Cytokines and Growth Factors
  3. Interleukin & Receptors
  4. IL-17 Receptor
  5. IL-17RE

IL-17RE  (白介素-17 受体 E)

IL-17RE 是 IL-17C 的特异性功能受体,主要由上皮细胞和淋巴细胞表达,如 Th17 细胞[1]。IL-17C/IL-17RE 轴在许多炎症和免疫疾病中发挥作用[2]。此外,在 IL-17RE 和任何其他 IL-17 细胞因子家族成员之间未发现相互作用。IL-17C 通过 IL-17RE-IL-17RA 复合物激活下游信号传导,以诱导编码抗菌肽和促炎分子的基因[3]
IL-17C 与上皮 IL-17C 源细胞上的 IL-17RA/RE 复合物的结合在上皮中形成自分泌环。与 IL-17A 一样,通过 IL-17RA/RE 的 IL-17C 信号传导使用衔接分子 ACT1。然后,信号级联通过 p38、ERK 和 JNK 的磷酸化激活 MAPK 通路,并通过 p65 亚基和 NF-κB 抑制剂 IκBα 的磷酸化激活 NF-κB 通路[2]。IL-17RE 调节 T 细胞活化,包括效应细胞因子(例如 IL-17A)的表达,并且 IL-17C/IL-17RE 轴在自身免疫疾病模型中增强效应 Th17 细胞的细胞因子表达。IL-17RE 也由肝脏驻留的 CD4+ T 细胞和自然杀伤 T 细胞高度表达,并与 IL-17C 一起增强自身免疫性肝炎中的 T 细胞功能。IL-17RE 的缺乏也为新月体肾毒性肾炎模型提供了保护[1]

Interleukin 17 receptor E (IL-17RE) is a specific functional receptor for IL-17C, and primarily expressed by epithelial cells and lymphocytes, such a Th17 cells[1]. IL-17C/IL-17RE-axis plays a role in many inflammatory and immune diseases[2]. Also, no interactions were found between IL-17RE and any of the other IL-17 cytokine family members. IL-17C activated downstream signaling through IL-17RE-IL-17RA complex for the induction of genes encoding antibacterial peptides as well as proinflammatory molecules[3].
Binding of IL-17C to the IL-17RA/RE complex on the epithelial IL-17C-source cells forms an autocrine loop in the epithelium. Like IL-17A, IL-17C signaling through IL-17RA/RE employs the adaptor molecule ACT1. The signaling cascade then activates the MAPK pathway by phosphorylation of p38, ERK, and JNK as well as the NF-κB pathway by phosphorylation of the p65 subunit and the NF-κB inhibitor IκBα[2]. IL-17RE meditates T cell activation, including the expression of effector cytokines (e.g. IL-17A), and the IL-17C/IL-17RE-axis enhances the expression of cytokine by effector Th17 cells in a in a model of autoimmune disease. IL-17RE is also highly expressed by liver resident CD4+ T cells and natural killer T cells and augments T cell function in autoimmune hepatitis together with IL-17C. Deficiency of IL-17RE also provides protection in a model of crescentic nephrotoxic nephritis[1].

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