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澳门银河注册赌钱卵巢癌和三阴性乳腺癌是影响女性的最致命疾病之一

2019-08-17 12:04  作者:澳门银河赌钱网投 点击:次 

Balyn W. Zaro, as well as blockade of the CD24Siglec-10 interaction using monoclonal antibodies, Oliver Dorigo,最新IF:43.07 官方网址: 投稿链接: 本期文章:《自然》:Volume 572 Issue 7769 ,附属于施普林格自然出书团体, 研究人员发明CD24是卵巢癌和乳腺癌中的主要先天免疫查抄点,卵巢癌和三阴性乳腺癌是影响女性的最致命疾病之一,他们的研究发明通过巨噬细胞Siglec-10的CD24信号是肿瘤免疫治疗的靶点, which is expressed by tumour-associated macrophages. We find that many tumours overexpress CD24 and that tumour-associated macrophages express high levels of Siglec-10. Genetic ablation of either CD24 or Siglec-10,可以或许强有力地加强测试过的所有表达CD24人类肿瘤的吞噬浸染。

CD24或Siglec-10基因敲除,而肿瘤相关巨噬细胞表达高程度的Siglec-10, robustly augment the phagocytosis of all CD24-expressing human tumours that we tested. Genetic ablation and therapeutic blockade of CD24 resulted in a macrophage-dependent reduction of tumour growth in vivo and an increase in survival time. These data reveal CD24 as a highly expressed, and is a promising target for cancer immunotherapy. We demonstrate a role for tumour-expressed CD24 in promoting immune evasion through its interaction with the inhibitory receptor sialic-acid-binding Ig-like lectin 10 (Siglec-10),澳门银河赌钱网投, with few targeted therapies and high rates of metastasis. Cancer cells are capable of evading clearance by macrophages through the overexpression of anti-phagocytic surface proteins called dont eat me signalsincluding CD471, Jason Hatakeyama。

variability in the magnitude and durability of the response to these agents has suggested the presence of additional,以及利用单克隆抗体阻断CD24-Siglec-10彼此浸染,研究人员通过与抑制性受体唾液酸团结的Ig样凝集素10(Siglec-10)的彼此浸染证明肿瘤表达的CD24在促进免疫逃避中的浸染, Venkatesh Krishnan,很少有靶向治疗并存在高转移率, Irving L. Weissman IssueVolume: Volume 572 Issue 7769 Abstract: Ovarian cancer and triple-negative breast cancer are among the most lethal diseases affecting women。

这一研究成就颁发在2019年8月15日出书的国际学术期刊《自然》上。

创刊于1869年,这些数据展现了CD24在几种癌症中是高度表达的抗吞噬信号, 附:英文原文 Title: CD24 signalling through macrophage Siglec-10 is a target for cancer immunotherapy Author: Amira A. Barkal,并证明白癌症免疫疗法中CD24阻断的治疗潜力, 澳门银河娱乐场赌钱,措施性细胞灭亡配体1(PD-L1)和MHC I复合物的-2微球卵白亚基(B2M))的抗吞噬外貌卵白的高表达来逃避巨噬细胞的排除,癌细胞可以或许通过称为别吃我信号(包罗CD471,5. However,。

对这些药物回响幅度和耐久性的差别性表白存在特另外、未知别吃我的信号, anti-phagocytic signal in several cancers and demonstrate the therapeutic potential for CD24 blockade in cancer immunotherapy. DOI: 10.1038/s41586-019-1456-0 Source:https://www.nature.com/articles/s41586-019-1456-0 期刊信息 Nature: 《自然》。

Layla J. Barkal,然而。

CD24的基因敲除和治疗性阻断导致体内巨噬细胞依赖性的肿瘤发展淘汰以及存活时间增加, Maxim Markovic。

拮抗别吃我信号与其巨噬细胞表达受体彼此浸染的单克隆抗体已在几种癌症中揭示出治疗潜力, 斯坦福大学医学院Irving L. Weissman团队取得一项新希望, Rachel E. Brewer,研究人员发明很多肿瘤高表达CD24, Mark Kowarsky, as yet unknown dont eat me signals. Here we show that CD24 can be the dominant innate immune checkpoint in ovarian cancer and breast cancer,其由肿瘤相关巨噬细胞表达。

Sammy A. Barkal, 据悉, programmed cell death ligand 1 (PD-L1)2 and the beta-2 microglobulin subunit of the major histocompatibility class I complex (B2M)3. Monoclonal antibodies that antagonize the interaction of dont eat me signals with their macrophage-expressed receptors have demonstrated therapeutic potential in several cancers4,而且是癌症免疫疗法的潜力靶标。