For nonimmunologists, a daunting and rapidly evolving immunologic vocabulary, our incom-plete understanding of both normal and abnormal immune function, and multiple interrelated complex immune cellular pathways can be a barrier to using basic immunology to understand and improve care for patients with type 1 diabetes. Our task in this review is to introduce current immune concepts specifically relevant to type 1 diabetes. Because our understanding is not complete, as evidenced perhaps by our lack of standard immunotherapy to prevent type 1 diabetes, we can only provide a partial framework. Perhaps the simplest framework (which may be wrong) is to consider the development of type 1 diabetes as the balance between regulatory and effector T lymphocytes. We know that in the absence of a major portion of regulatory T lymphocytes in a rare syndrome caused by mutation of the FOXP3 gene, most infants (even neonates) develop type 1 diabetes. Central to the development of type 1 diabetes are T lymphocytes with specific T-cell receptors that recognize islet molecules. When a T-cell is activated through its receptor, it can orchestrate protection from infection or autoimmunity, depending on the target. Other T-cells can suppress or enhance autoimmunity (either in general or only for T lymphocytes in islets). The activation of a T-cell involves multiple different cell types and genes, as we will discuss.