Hamilton-Williams, EmmaPalmer, StephanieCharlton, BrettSlattery, Robyn2015-12-132015-12-130027-8424http://hdl.handle.net/1885/88531Type 1 diabetes occurs as a result of an autoimmune attack on the insulin-producing beta cells. Although CD8 T cells have been implicated both early and late in this process, the requirement for direct interaction between these cells and MHC class I on the beta cells has not been demonstrated. By using nonobese diabetic mice lacking beta cell class I expression, we show that both initiation and progression of insulitis proceeds unperturbed. However, without beta cell class I expression, the vast majority of these mice do not develop hyperglycemia. These findings demonstrate that a direct interaction between CD8 T cells and beta cells is not required for initiation or early disease progression. The requirement for class I on beta cells is a relatively late checkpoint in the development of diabetes.Keywords: beta 2 microglobulin; cre recombinase; cyclophosphamide; DNA; insulin; major histocompatibility antigen class 1; animal cell; animal experiment; animal model; animal tissue; article; cell interaction; controlled study; disease course; fluorescence activat Nonobese diabetic; Severe combined immunodeficient; T lymphocytes200310.1073/pnas.11319541002015-12-12