Open AccessType 1 diabetes induced by immune checkpoint inhibitors
Author(s) -
Rui Zhang,
Xiaoling Cai,
Liu Liu,
Xueyao Han,
Lig Ji
Publication year - 2020
Publication title -
chinese medical journal/chinese medical journal
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 0.537
H-Index - 63
eISSN - 2542-5641
pISSN - 0366-6999
DOI - 10.1097/cm9.0000000000000972
Subject(s) - medicine , type 2 diabetes , diabetic ketoacidosis , type 1 diabetes , diabetes mellitus , immune system , immunology , adverse effect , immunotherapy , disease , autoantibody , ipilimumab , cytotoxic t cell , nivolumab , endocrinology , antibody , biology , biochemistry , in vitro
With the increasing use of immune checkpoint inhibitors (ICI) including anti-cytotoxic T lymphocyte associated antigen-4 (CTLA-4) and anti-programmed cell death-1 (PD-1) in cancers, ICI-induced type 1 diabetes has been reported throughout the world. In this review, we aim to summarize the characteristics of this disease and discuss the mechanism of it. As an immune-related adverse event, type 1 diabetes developed after the administration of anti-PD-1 or anti-PD-ligand 1 (PD-L1) in the combination with or without anti-CTLA-4. It usually presented with acute onset, and 62.1% of the reported cases had diabetic ketoacidosis. Only a third of them had positive autoantibodies associated with type 1 diabetes. Susceptible HLA genotypes might be associated. T-cell-stimulation by blocking of the interaction of PD-1 and PD-L1 in pancreatic β cells was the main mechanism involved in the pathology. Insulin was the only effective treatment of ICI-induced type 1 diabetes. In conclusions, ICI-induced type 1 diabetes is a potentially life-threating adverse event after the immunotherapy of cancers. Screening and early recognition is important. Further investigation of the mechanism may help to better understand the pathology of type 1 diabetes.