AITRL/TNFSF18 蛋白, Mouse (HEK293, Fc)

AITRL, a type II transmembrane protein, is a ligand for glucocorticoid-induced TNFR-related protein (GITR). When AITRL binds to GITR, GITR can produce costimulatory signals that regulate T-cell proliferation and effector functions. GITR/AITRL interaction plays a role in the pathogenesis of tumor, inflammation, as well as autoimmune diseases^[1]. Besides, AITRL plays a role in endothelial cells (EC)-activation and increases STAT-1 phosphorylation and the expression of adhesion molecules (VCAM-1, ICAM-1)^[2]. AITRL/TNFSF18 Protein, Mouse (HEK293, Fc) is a recombinant mouse AITRL (T47-S173) with N-terminal hFc tag, which is expressed in HEK293.

GITRL (AITRL) 是一种 II 型跨膜蛋白，是糖皮质激素诱导的 TNFR 相关蛋白 (GITR) 的配体。GITR 是 TNFR 超家族的成员，在 T 细胞、自然杀伤细胞和一些骨髓细胞中表达^[1]。鼠 GITRL 已在树突状细胞 (DC)、单核细胞、巨噬细胞、B 细胞、内皮细胞、破骨细胞和小胶质细胞中检测到^[4]。
当GITRL与GITR结合时，GITR可以产生调节T细胞增殖和效应功能的共刺激信号。这种相互作用刺激 CD4⁺ Teff 和 Treg 细胞的增殖和细胞因子产生，并驱动 CD8⁺ T 细胞^[3]的抗肿瘤活性。此外，GITRL 在 EC 激活中发挥作用，并促进小鼠和人类的粘附，从而增加 STAT-1 磷酸化并增强 VCAM-1 和 ICAM-1 等粘附分子的表达^[2]。小鼠 GITRL 可以激活信号转导，包括在 DC 中诱导耐受效应，并在巨噬细胞中诱导促炎刺激^[7]。
小鼠 GITRL 与人类具有 < 55% 的共同氨基酸同一性。小鼠 GITRL 以二聚体形式存在^[4] GITR/GITRL 相互作用在肿瘤、炎症以及自身免疫性疾病的发病机制中发挥作用^[1]

AITRL (mouse, 5 μg/mL, 48 h) promotes the maturation of myeloid-derived suppressor cells (MDSCs) isolated from ESS mice^[5].
AITRL (mouse, 2 μg/mL, 72 h) provides moderate costimulation to Treg cell proliferation^[6].

AITRL (mouse, 2 mg/kg, i.v.) attenuates the suppressive effect of MDSCs in ESS mice^[5].

Mouse

HEK293

N-hFc

Q7TS55 (T47-S173)

240873  [NCBI]

50-60 kDa

Greater than 95% as determined by Tris-Bis PAGE.

无菌粉末

Lyophilized from 0.22 μm filtered solution in PBS (pH 7.4). Normally 8% trehalose is added as protectant before lyophilization.

<1 EU/μg, determined by LAL method.

It is not recommended to reconstitute to a concentration less than 100 μg/mL in ddH₂O.

Stored at -20°C for 2 years. After reconstitution, it is stable at 4°C for 1 week or -20°C for longer (with carrier protein). It is recommended to freeze aliquots at -20°C or -80°C for extended storage.

Room temperature in continental US; may vary elsewhere.

• [1]. Tian J, et al. The Role of GITR/GITRL Interaction in Autoimmune Diseases. Front Immunol. 2020 Oct 9;11:588682.  [Content Brief]

  [2]. Lacal PM, et al. Glucocorticoid-induced tumor necrosis factor receptor family-related ligand triggering upregulates vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 and promotes leukocyte adhesion. J Pharmacol Exp Ther. 2013 Oct;347(1):164-72.  [Content Brief]

  [3]. Wang F, et al. Structures of mouse and human GITR-GITRL complexes reveal unique TNF superfamily interactions. Nat Commun. 2021 Mar 2;12(1):1378.  [Content Brief]

  [4]. Placke T, et al. Glucocorticoid-induced TNFR-related (GITR) protein and its ligand in antitumor immunity: functional role and therapeutic modulation. Clin Dev Immunol. 2010;2010:239083.  [Content Brief]

  [5]. Tian J, et al. Increased GITRL Impairs the Function of Myeloid-Derived Suppressor Cells and Exacerbates Primary Sjögren Syndrome. J Immunol. 2019 Mar 15;202(6):1693-1703.  [Content Brief]

  [6]. Chen M, et al. IFN-β induces the proliferation of CD4+CD25+Foxp3+ regulatory T cells through upregulation of GITRL on dendritic cells in the treatment of multiple sclerosis. J Neuroimmunol. 2012 Jan 18;242(1-2):39-46.  [Content Brief]

  [7]. Nocentini G, et al. Pharmacological modulation of GITRL/GITR system: therapeutic perspectives. Br J Pharmacol. 2012 Apr;165(7):2089-99.  [Content Brief]