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.

中文翻译：

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在患有预先确​​定的炎症性肠病的患者中使用免疫检查点抑制剂：回顾性病例系列。

炎症性肠病 (IBD) 的病因尚未完全了解。然而，它被认为是遗传、免疫和环境因素的结果，包括肠道微生物组的变化。1,2 免疫检查点抑制剂 (ICI) 彻底改变了晚期癌症的治疗。它们通过促进细胞毒性 T 细胞存活和抗肿瘤作用来激活免疫系统。目前共有7个ICI获美国食品药品监督管理局批准，靶向细胞毒性T淋巴细胞相关蛋白4（ipilimumab）；抗程序性细胞死亡 1 (PD-1)（nivolumab、pembrolizumab 和 cemiplimab）或抗 PD 配体 1（atezolizumab、durvalumab 和 avelumab）。然而，通过激活免疫系统，这些药物也会导致脱靶炎症和自身免疫，包括 ICI 诱导的结肠炎，