Purpose of review
Type 1 diabetes (T1D) is commonly portrayed as an autoimmune disease, in which misguided T lymphocyte activities cause selective destruction of insulin-producing pancreatic β-cells. New findings suggest that the immunological picture might be more complex than previously imagined. This review will focus on the recent studies that provide new insight into the hypothesis that neutrophils might participate in T1D initiation and perpetuation.
Reduced circulating neutrophil counts associate with T1D in humans from the pre-diabetic to the onset phases. Additionally, a hitherto unacknowledged role for neutrophils in T1D pathogenesis has recently been demonstrated in mice with spontaneous autoimmune T1D.
Although these findings have yet to undergo the scrutiny of the scientific community, they suggest that neutrophils – in addition to macrophages, dendritic cells, and lymphocytes – may play a role in T1D immunopathology. Further research is needed, which might lead to the definition of new therapeutic strategies for a disease that to date has proved controllable but incurable.