
Anja Schmidt-Christensen
Assistant researcher

E2-2 Dependent Plasmacytoid Dendritic Cells Control Autoimmune Diabetes.
Author
Summary, in English
Autoimmune diabetes is a consequence of immune-cell infiltration and destruction of pancreatic β-cells in the islets of Langerhans. We analyzed the cellular composition of the insulitic lesions in the autoimmune-prone non-obese diabetic (NOD) mouse and observed a peak in recruitment of plasmacytoid dendritic cells (pDCs) to NOD islets around 8-9 weeks of age. This peak coincides with increased spontaneous expression of type-1-IFN response genes and CpG1585 induced production of IFN-α from NOD islets. The transcription factor E2-2 is specifically required for the maturation of pDCs, and we show that knocking out E2-2 conditionally in CD11c+ cells leads to a reduced recruitment of pDCs to pancreatic islets and reduced CpG1585 induced production of IFN-α during insulitis. As a consequence, insulitis has a less aggressive expression profile of the Th1 cytokine IFN-γ and a markedly reduced diabetes incidence. Collectively, these observations demonstrate a disease-promoting role of E2-2 dependent pDCs in the pancreas during autoimmune diabetes in the NOD mouse.
Department/s
- Autoimmunity
- Department of Experimental Medical Science
- Genomics, Diabetes and Endocrinology
- Stem Cell Center
Publishing year
2015-12-01
Language
English
Publication/Series
PLoS ONE
Volume
10
Issue
12
Links
Document type
Journal article
Publisher
Public Library of Science
Topic
- Immunology in the medical area
Status
Published
Project
- inflammatory events leading to autoimmune Diabetes
Research group
- Autoimmunity
- Genomics, Diabetes and Endocrinology
ISBN/ISSN/Other
- ISSN: 1932-6203