Immunopathology of Type 1 Diabetes

The autoimmune disease type 1 diabetes has multifactorial pathogenesis and is a heterogeneous disease. Many insights have been gained in mouse models that bear similarity to the human disease, and discoveries in both humans and mouse models have been complementary. While it is evident in the mouse models that there is a T cell attack on the insulin-producing cells of the pancreatic islets of Langerhans, in humans, at least in some individuals, not all the insulin-producing cells are destroyed and, even many years after diagnosis, some insulin-producing cells remain. It is also clear that T cells are not the only immune cells involved in the damage of the insulin-producing cells; B cells, and innate immune cells also appear to play a role. A plethora of new information suggests that while there is a genetic predisposition to develop diabetes, environmental influences, long implicated in this process, are also demonstrating clearer associations.

In this Research Topic, we aim to bring together current knowledge and to highlight recent advances in the field of immunology of human type 1 diabetes, as well as discoveries made in animal models that inform our understanding of this complex immunological disease. In addition, we will focus on new discoveries and understanding that may have impact on development of immune therapy, both for prevention as well as treatment of established type 1 diabetes.

We welcome Original Research, Mini Review, Perspective, Opinion articles focusing on, but not limited to, the following themes:

• recent advances in pathology that may include research in: insulitis, measurements of beta cell mass (including beta cell heterogeneity), and evidence of viral involvement in pathogenesis;
• advances in the roles of B cell in immunopathology of type 1 diabetes, including their role in the thymus and discussion relating to new single cell analysis;
• new research and discussion relating to single cell analysis and the potential for identification of new disease modifiers;
• new research on T cells;
• environmental influences focusing on gut bacteria linking to innate immunity and including innate immune cells such as innate lymphoid cells and innate immune molecules;
• pathways to beta cell death, including the role of free radicals and other mechanisms;
• common mechanisms and comparisons with other autoimmune diseases.

We acknowledge the initiation and support of this Research Topic by the International Union of Immunological Societies (IUIS). We hereby state publicly that the IUIS has had no editorial input in articles included in this Research Topic, thus ensuring that all aspects of this Research Topic are evaluated objectively, unbiased by any specific policy or opinion of the IUIS.