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靶向脆性X智力低下蛋白:癌症免疫治疗的新窗口。

Targeting FMRP: A new window for cancer immunotherapy.

作者信息

Zhang Yaguang, Wu Tong, Han Junhong

机构信息

State Key Laboratory of Biotherapy and Cancer Center, and Frontiers Science Center for Disease-Related Molecular Network West China Hospital Sichuan University Chengdu P. R. China.

Research Laboratory of Cancer Epigenetics and Genomics West China Hospital Sichuan University Chengdu P. R. China.

出版信息

MedComm (2020). 2023 Mar 21;4(2):e233. doi: 10.1002/mco2.233. eCollection 2023 Apr.

DOI:10.1002/mco2.233
PMID:36968189
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10030685/
Abstract

FMRP is regulated by Myc and is highly expressed in a variety of human and mouse tumor tissues.FMRP recruits Treg and M2 macrophages to form an immunosuppressive tumor microenvironment by IL3, PROS1 and exosomes.FMRP-KO up-regulates tumor cell secretion of CCL7, which directly activates and recruits CD8+ T cells.FMRP-KO recruits CCR5 and CXCR4 receptor-positive CD8 T cells indirectly by promoting M1 macrophages to secrete CCL5, CXCL9, and CXCL10.

摘要

脆性X智力低下蛋白(FMRP)受Myc调控,在多种人类和小鼠肿瘤组织中高表达。FMRP通过白细胞介素3(IL3)、蛋白S1(PROS1)和外泌体招募调节性T细胞(Treg)和M2巨噬细胞,形成免疫抑制性肿瘤微环境。FMRP基因敲除(FMRP-KO)上调肿瘤细胞分泌趋化因子配体7(CCL7),直接激活并招募CD8+T细胞。FMRP-KO通过促进M1巨噬细胞分泌CCL5、CXC趋化因子配体9(CXCL9)和CXC趋化因子配体10(CXCL10),间接招募C-C趋化因子受体5(CCR5)和C-X-C趋化因子受体4(CXCR4)阳性的CD8 T细胞。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64b5/10030685/e80cf4f24e76/MCO2-4-e233-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64b5/10030685/e80cf4f24e76/MCO2-4-e233-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64b5/10030685/e80cf4f24e76/MCO2-4-e233-g001.jpg

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A reality check of the accelerated approval of immune-checkpoint inhibitors.免疫检查点抑制剂加速批准的现实审视。
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