Abstrakt
Type 1 diabetes (T1D) is an autoimmune disease with multifactorial aetiology that involves an attack of self-reactive cytotoxic CD8 lymphocytes on insulin-producing beta cells in the pancreas. However, not only T lymphocytes contribute to the T1D pathophysiology.
Both innate and adaptive immunity mechanisms cooperate in the development of inflammation leading to autoimmune destruction. Innate immunity dysregulation is apparent not only in long-term treated T1D patients and is not associated with metabolic changes, suggesting that the changes are intrinsic and potentially determined genetically.
Since presymptomatic patients would benefit from early identification of the onset of the pathological processes leading to symptomatic T1D, we believe that thorough understanding the underlying mechanisms is crucial. Here, we focus on neutrophils and their products called neutrophil extracellular traps (NETs).
NET structures are predominantly composed of neutrophil DNA and antimicrobial proteins and are an important mechanism of antimicrobial defence; however, in recent years, NETs gained considerable attention in the field of autoimmune diseases as a source of potential autoantigens. They are able to induce IFNγ-producing T cells through activation of dendritic cells (DCs), since we show that T1D monocytes and DCs inappropriately react to the presence of DNA regardless of the origin, including microbial or endogenous sources, suggesting that aberrant recognition of DNA contained in NETs also participates in the inflammation associated.