医学
无容量
易普利姆玛
杜瓦卢马布
阿替唑单抗
彭布罗利珠单抗
炎症性肠病
免疫学
细胞毒性T细胞
免疫系统
银耳霉素
阿维鲁单抗
结肠炎
免疫检查点
免疫疗法
内科学
疾病
体外
生物化学
化学
作者
Manuel Bonfim Braga Neto,Guilherme Piovezani Ramos,Edward V. Loftus,William A. Faubion,Laura E. Raffals
标识
DOI:10.1016/j.cgh.2020.06.031
摘要
The etiology of inflammatory bowel disease (IBD) has yet to be fully understood; however, it is thought to be a result of genetic, immunologic, and environmental factors, including changes in the gut microbiome.1,2 Immune checkpoint inhibitors (ICI) have revolutionized treatment of advanced cancer. They activate the immune system by promoting cytotoxic T-cell survival and antitumor effects. A total of 7 ICIs currently are approved by the United States Food and Drug Administration, and target cytotoxic T lymphocyte–associated protein 4 (ipilimumab); anti–programmed cell death 1 (PD-1) (nivolumab, pembrolizumab, and cemiplimab), or anti–PD-ligand 1 (atezolizumab, durvalumab, and avelumab). However, by activating the immune system, these medications also can lead to off-target inflammation and autoimmunity, including ICI-induced colitis, which has been reported in up to 13.6% of patients.3
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