title: Eosinophils from patients with type 1 diabetes mellitus express high level of myeloid alpha-defensins and myeloperoxidase.
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 CD15(dull)/CD14(weak) 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 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.
authors.affiliation: Laboratory of Immunobiology, Institute of Molecular Genetics AS CR, Prague, Czech Republic.
authors.forename: Aleš
authors.initials: A
authors.lastname: Neuwirth
authors.forename: Jan
authors.initials: J
authors.lastname: Dobeš
authors.forename: Jana
authors.initials: J
authors.lastname: Oujezdská
authors.forename: Ondřej
authors.initials: O
authors.lastname: Ballek
authors.forename: Martina
authors.initials: M
authors.lastname: Benešová
authors.forename: Zdeněk
authors.initials: Z
authors.lastname: Sumník
authors.forename: Jana
authors.initials: J
authors.lastname: Včeláková
authors.forename: Stanislava
authors.initials: S
authors.lastname: Koloušková
authors.forename: Barbora
authors.initials: B
authors.lastname: Obermannová
authors.forename: Michal
authors.initials: M
authors.lastname: Kolář
authors.forename: Kateřina
authors.initials: K
authors.lastname: Stechová
authors.forename: Dominik
authors.initials: D
authors.lastname: Filipp
mesh_terms: D000293:Adolescent; D000328:Adult; D015551:Autoimmunity; D002648:Child; D002675:Child, Preschool; D003922:Diabetes Mellitus, Type 1 / Q000097:blood / Q000235:genetics / Q000276:immunology*; D004804:Eosinophils / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D005434:Flow Cytometry; D015870:Gene Expression; D006801:Humans; D007108:Immune Tolerance; D007113:Immunity, Innate; D050417:Insulin-Secreting Cells / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D016256:Lewis X Antigen / Q000276:immunology; D018950:Lipopolysaccharide Receptors / Q000276:immunology; D009195:Peroxidase / Q000097:blood / Q000235:genetics / Q000276:immunology*; D012333:RNA, Messenger / Q000096:biosynthesis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D023084:alpha-Defensins / Q000097:blood / Q000235:genetics / Q000276:immunology*
chemical_list: D016256:Lewis X Antigen; D018950:Lipopolysaccharide Receptors; D012333:RNA, Messenger; D023084:alpha-Defensins; D009195:Peroxidase