The Innate Immune System as a Driver of Diabetes and its Complications

Type 1 diabetes (T1D) and type 2 diabetes (T2D) have traditionally been viewed as distinct disorders. T1D is an autoimmune disease in which the classical view is that antigen-specific T cells recognize and attack insulin-producing pancreatic beta cells. In contrast, T2D is primarily considered a metabolic disorder, where chronic stress on islet beta cells leads to their dysfunction and eventually inability to maintain euglycemia, either due to profound insulin resistance or diminished insulin production from beta-cell exhaustion.

Thanks to recent discoveries and advances, it is now generally accepted that T1D can be influenced and aggravated by metabolic disturbances and that T2D has a component of inflammation and genetic predisposition playing a role in the disease. Moreover, a growing body of scientific research suggests that several intricate components of the innate immune system play a role in the onset and progression of both T1D and T2D. Furthermore, recent literature suggests that the innate immune system plays a critical role in their complications, cardiovascular and others, that are caused not only by poor glycemic control but also by a low-key systemic inflammation. Recent developments have expanded the mechanisms and cells that operate in the innate immune response, e.g., trained immunity, non-classical HLA class I molecules, and innate lymphocytes.

This topic welcomes studies investigating the role of different cell types and components of the innate immune system in T1D and T2D initiation, progression, and associated complications.

We encourage submissions of original research, reviews, mini-reviews, perspectives, and brief research reports.