The browser you are using is not supported by this website. All versions of Internet Explorer are no longer supported, either by us or Microsoft (read more here: https://www.microsoft.com/en-us/microsoft-365/windows/end-of-ie-support).

Please use a modern browser to fully experience our website, such as the newest versions of Edge, Chrome, Firefox or Safari etc.

Default user image.

Anja Schmidt-Christensen

Assistant researcher

Default user image.

E2-2 Dependent Plasmacytoid Dendritic Cells Control Autoimmune Diabetes.

Author

  • Lisbeth Hansen
  • Anja Schmidt-Christensen
  • Shashank Gupta
  • Nina Fransén Pettersson
  • Tine Hannibal
  • Boris Reizis
  • Pere Santamaria
  • Dan Holmberg

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

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