Immune checkpoint therapy and type 1 diabetes

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• 作者：Hiroshi Ikegami ; Yumiko Kawabata ; Shinsuke Noso
• 关键词：Type 1 diabetes ; Fulminant type 1 diabetes ; Autoimmune disease ; Immune checkpoint ; Programmed death 1 (PD ; 1) ; Cytotoxic T ; lymphocyte associated protein 4 (CTLA4)
• 刊名：Diabetology International
• 出版年：2016
• 出版时间：September 2016
• 年：2016
• 卷：7
• 期：3
• 页码：221-227
• 全文大小：648 KB
• 刊物主题：Diabetes; Metabolic Diseases; Endocrinology;
• 出版者：Springer Japan
• ISSN：2190-1686
• 卷排序：7

文摘

Type 1 diabetes is caused by destruction of insulin-producing beta cells of the pancreas. The etiology of type 1 diabetes is immune-mediated by either an organ-specific autoimmune mechanism in autoimmune type 1 diabetes or a still unknown but probably immune-mediated mechanism in fulminant type 1 diabetes. Immunomodulation is therefore expected to accelerate or inhibit type 1 diabetes. Recent progress in anti-cancer therapy by immune-checkpoint blockade, such as anti-PD-1 and anti-CTLA4 monoclonal antibodies, has markedly improved the prognosis of patients with advanced cancers. These drugs activate anti-tumor immunity by blocking inhibitory signals of T lymphocytes. Activation of immunological pathways, however, is expected to accelerate immune-mediated diseases. In fact, the development of autoimmune-thyroid diseases and type 1 diabetes, including fulminant type 1 diabetes, has been reported in patients treated with immune checkpoint blockers. The development of fulminant type 1 diabetes is a major concern because of its abrupt onset and very rapid progression, leading to death unless proper treatment is initiated immediately after diagnosis. In this review, the development of type 1 diabetes with immune-checkpoint therapy and its etiological background are discussed.