New Insights into the Pathogenesis of Type 1 Diabetes

Dear Colleagues,

Insulin-dependent diabetes mellitus (type 1 diabetes, T1D) is a multifactorial autoimmune disease with a strong genetic component. The disorder occurs in individuals genetically predisposed to human leukocyte antigen (HLA) as a consequence of organ-specific immune destruction of the insulin-producing cells in the islets of Langerhans within the pancreas. As a genetic background, dominant loci within the major histocompatibility complex (MHC) and the HLA region predisposing to the disease were recognized in both the NOD and human disease.

The pathogenesis of this multifactorial disorder requires the contribution of genetics, still-unknown environmental factors, and stochastic events. It is generally recognized that T1D derives from a breakdown in immune regulation that leads to the expansion of autoreactive CD4⁺ and CD8⁺ T cells, autoantibody-producing B lymphocytes, and activation of the innate immune system.

In this Special Issue, we discuss recent discoveries on the pathogenesis of T1D that constitute the background for the development of novel immunotherapies.

Dr. Alessandra Fierabracci
Guest Editor

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• type 1 diabetes
• insulin-dependent diabetes mellitus
• human leukocyte antigen (HLA)
• pathogenesis