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img  1:  Immune checkpoint therapy and type 1 diabetes.
 
著者: Hiroshi Ikegami, Yumiko Kawabata, Shinsuke Noso
雑誌名: Diabetol Int. 2016 Sep;7(3):221-227. doi: 10.1007/s13340-016-0276-9. Epub 2016 Jul 5.
Abstract/Text 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.

PMID 30603267  Diabetol Int. 2016 Sep;7(3):221-227. doi: 10.1007/s13340-016-0276-9. Epub 2016 Jul 5.
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