Author/Authors :
Neuwirth، نويسنده , , Ale? and Dobe?، نويسنده , , Jan and Oujezdsk?، نويسنده , , Jana and Ballek، نويسنده , , Ond?ej and Bene?ov?، نويسنده , , Martina and ?umn?k، نويسنده , , Zden?k and V?el?kov?، نويسنده , , Jana and Kolou?kov?، نويسنده , , Stanislava and Obermannov?، نويسنده , , Barbora and Kol??، نويسنده , , Michal and ?techov?، نويسنده , , Kate?ina and Filipp، نويسنده , , Dominik، نويسنده ,
Abstract :
Type 1 diabetes (T1D) is an autoimmune disease caused by T-cell mediated destruction of pancreatic beta cells. Recently, small cationic α-defensin molecules have been implicated in the pathogenesis of certain inflammatory and autoimmune diseases. The purpose of this study was to assess the α-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 α-defensin mRNAs in their capillary blood. Quantitative RT-PCR performed on FACS-sorted granulocytes identified CD15dull/CD14weak population as the cellular source of α-defensins. Surprisingly, this granulocyte subpopulation displayed augmentation of α-defensin expression in all T1D patients tested. The determination of cell surface markers, expression of cell-specific genes and confocal microscopy identified CD15dull/CD14weak 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.
Keywords :
Type 1 diabetes , ?-defensin , Myeloperoxidase , Granulocyte , Eosinophil