Immune Checkpoint Inhibitor-Associated Colitis and Hepatitis.
Immune Checkpoint Inhibitor-Associated Colitis and Hepatitis.
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DOI：
10.1038/s41424-018-0049-9
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发表时间：
2018-09-19
影响因子：
3.6
通讯作者：
Tai AW
中科院分区：
文献类型：
--
作者：
Reddy HG;Schneider BJ;Tai AW
免疫检查点抑制剂（ICPIs）是靶向抗癌免疫应答下调因子的单克隆抗体：细胞毒性T淋巴细胞抗原-4、程序性细胞死亡蛋白-1及其配体PD-L1。ICPIs现在被批准用于治疗各种恶性肿瘤，在转移性环境中的持久反应率远远超过传统化疗的预期。ICPIs还与罕见但严重的免疫相关不良事件有关，这是由于免疫系统过度激活，可能影响任何器官，包括胃肠道和肝脏。随着ICPI在肿瘤学中的使用不断增加，胃肠病学家和肝病学家将经常遇到ICPI相关的结肠炎和肝炎。本文将重点介绍ICPI相关性结肠炎和肝炎的诊断和治疗。我们还将比较ICPI相关毒性与散发性炎症性肠病和自身免疫性肝病。
Immune checkpoint inhibitors (ICPIs) are monoclonal antibodies that target downregulators of the anti-cancer immune response: cytotoxic T-lymphocyte antigen-4, programmed cell death protein-1, and its ligand PD-L1. ICPIs are now approved for the treatment of a wide array of malignancies, with rates of durable responses in the metastatic setting far exceeding what would be expected from conventional chemotherapy. ICPIs have also been associated with rare but serious immune-related adverse events due to over-activation of the immune system that can affect any organ, including the gastrointestinal tract and liver. As the use of ICPIs in oncology continues to increase, ICPI-associated colitis and hepatitis will be encountered frequently by gastroenterologists and hepatologists. This review will focus on the diagnosis and management of ICPI-associated colitis and hepatitis. We will also compare these ICPI-related toxicities with sporadic inflammatory bowel disease and autoimmune liver disease.
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PD-1和PD-L1检查点信号传导抑制癌症免疫疗法：机制，组合和临床结果。
影响因子：
5.6
作者：
Alsaab HO;Sau S;Alzhrani R;Tatiparti K;Bhise K;Kashaw SK;Iyer AK
通讯作者：
Iyer AK
影响因子：
3.4
作者：
Kim, Kyung Won;Ramaiya, Nikhil H.;Ibrahim, Nageatte
通讯作者：
Ibrahim, Nageatte
影响因子：
50.5
作者：
Menzies, A. M.;Johnson, D. B.;Long, G. V.
通讯作者：
Long, G. V.
影响因子：
16.6
作者：
Dubin K;Callahan MK;Ren B;Khanin R;Viale A;Ling L;No D;Gobourne A;Littmann E;Huttenhower C;Pamer EG;Wolchok JD
通讯作者：
Wolchok JD
影响因子：
28.4
作者：
Johnson, Douglas B.;Sullivan, Ryan J.;Clark, Joseph I.
通讯作者：
Clark, Joseph I.