Figure 2.

NK cells in the pathogenesis of virus-induced type 1 diabetes during persistent CV-B infection: possible mechanisms. Persistent CV-B infection inhibits the expression of HLA class I molecules on human pancreatic beta cells. NK cells induce apoptosis of virus-infected cells that have altered or downregulated surface expression of HLA class I molecules. Apoptotic beta cells can direct immune response towards autoimmunity through autoreactive T lymphocyte activation. Moreover, IFN-α produced by infected beta cells enhances NK cells cytolytic activity while IFN-γ produced by NK cells damages beta cells (infected and non-infected) by direct cytotoxicity. IFN-α and IFN-γ are able to upregulate HLA class I expression on beta cells leading to increase immune recognition and activation of autoreactive T cells and hence autoimmunity towards beta cells.