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CD4 和 CD8 T 淋巴细胞在控制肿瘤生长中的相互作用。

CD4 and CD8 T lymphocyte interplay in controlling tumor growth.

机构信息

Clinic for Gastroenterology, Hepatology, and Endocrinology, Hannover Medical School, Carl Neuberg Str. 1, 30625, Hannover, Germany.

出版信息

Cell Mol Life Sci. 2018 Feb;75(4):689-713. doi: 10.1007/s00018-017-2686-7. Epub 2017 Oct 14.

DOI:10.1007/s00018-017-2686-7
PMID:29032503
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5769828/
Abstract

The outstanding clinical success of immune checkpoint blockade has revived the interest in underlying mechanisms of the immune system that are capable of eliminating tumors even in advanced stages. In this scenario, CD4 and CD8 T cell responses are part of the cancer immune cycle and both populations significantly influence the clinical outcome. In general, the immune system has evolved several mechanisms to protect the host against cancer. Each of them has to be undermined or evaded during cancer development to enable tumor outgrowth. In this review, we give an overview of T lymphocyte-driven control of tumor growth and discuss the involved tumor-suppressive mechanisms of the immune system, such as senescence surveillance, cancer immunosurveillance, and cancer immunoediting with respect to recent clinical developments of immunotherapies. The main focus is on the currently existing knowledge about the CD4 and CD8 T lymphocyte interplay that mediates the control of tumor growth.

摘要

免疫检查点阻断的卓越临床成功重新激发了人们对免疫系统潜在机制的兴趣,这些机制即使在晚期也能够消除肿瘤。在这种情况下,CD4 和 CD8 T 细胞反应是癌症免疫周期的一部分,这两种细胞群都显著影响临床结果。一般来说,免疫系统已经进化出几种机制来保护宿主免受癌症的侵害。在癌症发展过程中,每种机制都必须被破坏或逃避,才能使肿瘤生长。在这篇综述中,我们概述了 T 淋巴细胞对肿瘤生长的控制,并讨论了涉及免疫系统的肿瘤抑制机制,如衰老监测、癌症免疫监视和癌症免疫编辑,以及免疫疗法的最新临床进展。重点是目前关于介导肿瘤生长控制的 CD4 和 CD8 T 淋巴细胞相互作用的现有知识。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bbf/11105510/77fb4f2b327d/18_2017_2686_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bbf/11105510/281e0bc4ba61/18_2017_2686_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bbf/11105510/77fb4f2b327d/18_2017_2686_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bbf/11105510/281e0bc4ba61/18_2017_2686_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bbf/11105510/77fb4f2b327d/18_2017_2686_Fig2_HTML.jpg

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