程序性死亡配體1抗體/PD-L1 Antibody |
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產(chǎn)品名稱 ： 程序性死亡配體1抗體/PD-L1 Antibody
產(chǎn)品類別 ： IVD診斷抗體原料
品 牌 ： GenomeMe
貨 號(hào) ： IHC411
規(guī) 格 ： 0.1ml/1ml
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詳細(xì)信息 |
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背景描述Description：
程序性死亡配體1(PD-L1)又稱CD274或B7同源物1(B7-H1)，是一種跨膜蛋白，通過與程序性死亡-1(PD-1)受體的結(jié)合，抑制免疫系統(tǒng)，使腫瘤細(xì)胞抵抗CD8+T細(xì)胞介導(dǎo)的殺傷。PD-L1的過度表達(dá)可能使癌細(xì)胞逃避宿主免疫系統(tǒng)的作用。在腎細(xì)胞癌中，PD-L1的表達(dá)上調(diào)與腫瘤侵襲性和死亡風(fēng)險(xiǎn)增加有關(guān)，而在卵巢癌中，PD-L1的高表達(dá)會(huì)導(dǎo)致明顯的不良預(yù)后。PD-L1還與系統(tǒng)性紅斑狼瘡和皮膚黑色素瘤有關(guān)。當(dāng)與CD8+腫瘤浸潤淋巴細(xì)胞密度聯(lián)合考慮時(shí)，PD-L1的表達(dá)水平可能是預(yù)測多種癌癥類型的有用指標(biāo)，包括III期非小細(xì)胞肺癌、激素受體陰性乳腺癌和前哨淋巴結(jié)黑色素瘤。
Programmed Death-Ligand 1 (PD-L1), also known as CD274 or B7 Homolog 1 (B7-H1), is a transmembrane protein involved in suppressing the immune system and rendering tumor cells resistant to CD8+ T cell-mediated lysis through binding of the Programmed Death-1 (PD-1) receptor. Overexpression of PD-L1 may allow cancer cells to evade the actions of the host immune system. In renal cell carcinoma, upregulation of PD-L1 has been linked to increased tumor aggressiveness and risk of death, and, in ovarian cancer, higher expression of this protein has lead to significantly poorer prognosis. PD-L1 has also been linked to systemic lupus erythematosus and cutaneous melanoma. When considered in adjunct with CD8+ tumor-infiltrating lymphocyte density, expression levels of PD-L1 may be a useful predictor of multiple cancer types, including stage III non-small cell lung cancer, hormone receptor negative breast cancer, and sentinel lymph node melanoma.
Specifications：
Clone IHC411
Source Rabbit Monoclonal
Positive Control Tonsil, Lung Adenocarcinoma
Dilution Range 1:50-1:200
參考文獻(xiàn)References:
Ostrand-Rosenberg S, et al. J Immunol. 2014; 193:3835-41.
Tokito T, et al. Eur J Cancer. 2016; 55:7-14.
Park IH, et al. Clin Breast Cancer. 2016; 16:51-8.
Kakavand H, et al. Mod Pathol. 2015; 28: 1535-44.
Xia B, et al. Immunotherapy. 2016; 8:279-98.
Patel SP, et al. Mol Cancer Ther. 2015; 14:847-56.
Singh BP, et al. Cancers (Basel). 2016; 8.
Chemnitz JM, et al. J Immunol. 2004; 173:945–54.
Thompson RH, et al. Proc Natl Acad Sci USA. 2004; 101:17174–9.
Hamanishi J, et al. Proc Natl Acad Sci USA. 2007; 104:3360–5.
Mozaffarian N, et al. Rheumatology, 2008; 47:1335–41.
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