IL-10R alpha 蛋白, Mouse (HEK293, Fc)

IL-10R alpha protein is an IL10 cytokine surface receptor that is involved in IL10-mediated inflammation and immune regulation and inhibits the synthesis of pro-inflammatory cytokines. IL-10R alpha Protein, Mouse (HEK293, Fc) is expressed by HEK 293cells with a hFc tag at the C-terminus^[1].

IL-10Rα是II型细胞因子受体的配体结合亚基，由2个α和2个β亚基组成，主要在造血细胞中表达，例如B细胞、T细胞、NK细胞、单核细胞和巨噬细胞，但不在非造血细胞中表达。-造血细胞，如成纤维细胞或内皮细胞^[1]。
IL-10R α 与配体结合并导致 β 亚基发生构象变化，从而导致 β 亚基也发生构象变化结合 IL-10，形成异四聚体，从而激活 JAK1 和 TYK2 激酶的信号复合物。在这种情况下，JAK1 与 α 亚基结合，TYK2 与 β 亚基结合，磷酸化 IL10R α 细胞内结构域中的特定酪氨酸残基。这进一步导致转录因子 STAT3 的磷酸化和激活，从而使 STAT3 单体二聚化进入细胞核并诱导靶基因的转录表达^[1]。
IL-10R α 参与抑制炎症反应和 Th 1 细胞介导的免疫反应，还调节中性粒细胞功能反应。此外，IL10R α 介导的 STAT3 激活也会抑制饥饿诱导的自噬^[2]。

IL-1R alpha expression levels is low in naive (CD45RBhi), memory/effector (Treg cell-depleted CD45RBlo), and nTreg CD4 T cells, but IL-1Rα expression levels can be upregulated by in vitro stimulation with anti-CD3 and CD28 antibodies^[3].

IL1R alpha expression is low in naive CD4⁺ T cells but is efficiently induced in small intestinal Th17 cells of anti-CD3-treated mice^[4].
IL-1R alpha can be induced by IFN-γ in a mouse model of colitis DSS, while deletion of IL-1R alpha in an epithelial-specific IL-1R alpha knockout (KO) mouse model leads to increased colitis, suggesting an important role for epithelial IL-1R alpha in mucosal integrity and possibly barrier function^[5].

Mouse

HEK293

C-hFc

Q61727/NP_032374.1 (L17-N238)

16154  [NCBI]

Approximately 52.7 kDa

Greater than 95% as determined by reducing SDS-PAGE.

溶液

Supplied as a 0.2 μm filtered solution of PBS, pH 7.4.

<1 EU/μg, determined by LAL method.

N/A.

Stored at -80°C for 1 year. It is stable at -20°C for 3 months after opening. It is recommended to freeze aliquots at -80°C for extended storage. Avoid repeated freeze-thaw cycles.

Shipping with dry ice.

• [1]. Dror S Shouval, et al. Interleukin 10 receptor signaling: master regulator of intestinal mucosal homeostasis in mice and humans. Adv Immunol. 2014;122:177-210.  [Content Brief]

  [2]. J Shi, et al. IL10 inhibits starvation-induced autophagy in hypertrophic scar fibroblasts via cross talk between the IL10-IL10R-STAT3 and IL10-AKT-mTOR pathways. Cell Death Dis. 2016 Mar 10;7(3):e2133.  [Content Brief]

  [3]. Masahito Kamanaka, et al. Memory/effector (CD45RB(lo)) CD4 T cells are controlled directly by IL-10 and cause IL-22-dependent intestinal pathology. J Exp Med. 2011 May 9;208(5):1027-40.  [Content Brief]

  [4]. Samuel Huber, et al. Th17 cells express interleukin-10 receptor and are controlled by Foxp3⁻ and Foxp3+ regulatory CD4+ T cells in an interleukin-10-dependent manner. Immunity. 2011 Apr 22;34(4):554-65.  [Content Brief]

  [5]. Douglas J Kominsky, et al. IFN-γ-mediated induction of an apical IL-10 receptor on polarized intestinal epithelia. J Immunol. 2014 Feb 1;192(3):1267-76.  [Content Brief]