Type 1 diabetes (T1D) is an autoimmune disease caused by T-cell mediated destruction of pancreatic beta cells. Recently, small cationic alpha-defensin molecules have been implicated in the pathogenesis of certain inflammatory and autoimmune diseases.
The purpose of this study was to assess the alpha-defensin expression in patients with T1D and elucidate the cellular source of their production. Our results show that 30% of patients exhibit increased levels of alpha-defensin mRNAs in their capillary blood.
Quantitative RT-PCR performed on FACS-sorted granulocytes identified CD15(dull)/CD14(weak) population as the cellular source of alpha-defensins. Surprisingly, this granulocyte subpopulation displayed augmentation of alpha-defensin expression in all T1D patients tested.
The determination of cell surface markers, expression of cell-specific genes and confocal microscopy identified CD15(dull)/CD14(weak) cells as eosinophils. The presence of transcriptionally active eosinophils in diabetic patients suggests that eosinophils could be a part of an intricate innate immune cellular network involved in the development of diabetes.