• type 1 diabetes mellitus;
  • NOD mice;
  • dendritic cells;
  • NFkB

In type 1 diabetes, dendritic cells (DCs) display defective phenotype and function and possibly play crucial roles in the pathogenesis of this disease. In the present study, we compared transcription profiles of CD11c+ bone marrow (BM)-derived DCs from NOD mice with those from NON mice, focusing on the NF-κB/Rel family members and associated molecules. The BMDCs from NOD mice displayed reduced mRNA expressions of NF-κB components, p65, p50, p52, and RelB, compared to NON mice: the proportions of each molecule relative to those of NON DCs were 53.9, 54.1, 54.0, and 37.0%, respectively, which were accompanied with lowered expressions of downstream immunomodulatory molecules, including IL-6, CD80, CD86, 4-1BB, and CD40. The reduction of NF-κB components possibly underlies the defective phenotype and function of DCs from NOD mice, and could predispose to autoimmunity.