Reduced interferon‐α production by dendritic cells in type 1 diabetes does not impair immunity to influenza virus

Summary The increased risk and persistence of infections in diabetic condition is probably associated with defects in the cellular immune responses. We have previously shown a decrease in the production of interferon ( IFN )‐α by dendritic cells ( DC s) in diabetic subjects. The basal level of IFN ‐α in splenic plasmacytoid DC s (p DC s) is also lower in non‐obese diabetic ( NOD ) mice compared to prediabetic mice. The objective of this study was to analyse the ability of diabetic mice to mobilize innate and CD 8 + T cell‐mediated immune response to influenza A virus ( IAV ) with the live influenza A / P uerto R ico/8/1934 H 1 N 1 ( PR 8) strain or with its immunodominant CD 8 + T cell epitopes. We found that following immunization with IAV , the level of IFN ‐α in diabetic mice was increased to the level in prediabetic mice. Immunization of NOD mice with the immunodominant IAV PR 8 peptide induced clonal expansion of IFN ‐γ‐producing CD 8 + T cells similar to the response observed in prediabetic mice. Thus, diabetic and prediabetic NOD mice have a similar capacity for IFN ‐α and IFN ‐γ production by p DC s and CD 8 + T cells, respectively. Therefore, the DC‐related immune defect in diabetic NOD mice does not impair their capacity to develop an effective immune response to IAV . Our results suggest that reduced IFN ‐α production by diabetic human and mouse DC s is not an impediment to an effective immunity to IAV in type 1 diabetic subjects vaccinated with live attenuated influenza vaccine.