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The role of perforin and granzymes in diabetes Thomas HE; Trapani JA; Kay TWCell Death Differ 2010[Apr]; 17 (4): 577-85Type 1 diabetes results from autoimmune destruction of pancreatic beta-cells by CD8(+) T cells. The requirement for CD8(+) T cells implicates perforin and granzymes as effectors of tissue destruction. Diabetogenic cytotoxic T cells kill beta-cells by the perforin/granzyme pathway in vitro. In the non-obese diabetic mouse model of type I diabetes, perforin deficiency results in a highly significant reduction in disease, indicating a direct role for perforin in beta-cell death in vivo, although other cell death pathways must account for the residual diabetes in perforin-deficient mice. Perforin and granzyme B are also important in allogeneic destruction of islets. The dominant role of the perforin/granzyme pathway in beta-cell destruction in type I diabetes and allogeneic islet graft rejection make this pathway an important target for blockade in future therapies for type I diabetes. In addition, granzymes have a newly recognized role in inflammation, a feature of both type I and II diabetes, suggesting their role should be further explored in both the common forms of diabetes.|Animals[MESH]|Cell Death/immunology[MESH]|Diabetes Mellitus, Type 1/*enzymology/*immunology/physiopathology[MESH]|Graft Rejection/immunology[MESH]|Granzymes/*physiology[MESH]|Humans[MESH]|Inflammation/enzymology/immunology/physiopathology[MESH]|Insulin-Secreting Cells/immunology[MESH]|Perforin/*physiology[MESH]|Signal Transduction/immunology[MESH]|T-Lymphocytes, Cytotoxic/*enzymology/*immunology[MESH] |
