Journal for immunotherapy of cancer · 2025
Autoimmune origin for immune checkpoint inhibitor-diabetes revealed by deep immune phenotyping of the pancreas.
СтатьяКлинический случайНазвание и аннотация: Перевод в очереди
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Quandt Zoe, Young Arabella, Barlow Graham Larson, Smith Jennifer A, Kusmartseva Irina, Dong Shen, Shapiro Melanie R, Kang Jee Hye, Felton Jamie L, Nguyen Vinh Q, Szot Greg, Hassoun Assad A, Perdigoto Ana Luisa, Herold Kevan C, Nolan Garry, Bollyky Paul L, Brusko Todd M, Nakayama Maki, Cooper Stewart, Anderson Mark S
Аннотация
Immune checkpoint inhibitor-diabetes (CPI-D) is an acute and non-resolving immune-related adverse event (irAE) initiated primarily by disrupting the programmed death-1 (PD-1)/programmed death-ligand 1 (PD-L1) axis with monoclonal antibodies. A major limitation in understanding CPI-D is the lack of access to pancreatic tissue from patients experiencing this complication. We report a unique patient with no prior history of diabetes or autoimmune disease whose treatment with CPI for metastatic melanoma was complicated by CPI-D requiring insulin therapy. The patient then went on to develop pancreatic cancer. In the setting of the pancreatic cancer treatment, we were able to perform detailed single-cell RNA sequencing and immunophenotyping within the surgically resected pancreas. This revealed substantial lymphocytic infiltration associated with the islets, suggestive of an autoimmune rather than autoinflammatory mechanistic origin for CPI-D.