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E2-2 Dependent Plasmacytoid Dendritic Cells Control Autoimmune Diabetes.

Hansen, Lisbeth LU ; Schmidt-Christensen, Anja LU orcid ; Gupta, Shashank LU ; Fransén Pettersson, Nina LU ; Hannibal, Tine LU ; Reizis, Boris ; Santamaria, Pere and Holmberg, Dan LU (2015) In PLoS ONE 10(12).
Abstract
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... (More)
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. (Less)
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author
; ; ; ; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
PLoS ONE
volume
10
issue
12
article number
e0144090
publisher
Public Library of Science (PLoS)
external identifiers
  • pmid:26624013
  • wos:000365891600091
  • scopus:84956530874
  • pmid:26624013
ISSN
1932-6203
DOI
10.1371/journal.pone.0144090
project
inflammatory events leading to autoimmune Diabetes
language
English
LU publication?
yes
id
bc7287a7-d860-4649-891c-413073a2db0a (old id 8505936)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/26624013?dopt=Abstract
date added to LUP
2016-04-01 13:42:02
date last changed
2024-04-24 12:01:58
@article{bc7287a7-d860-4649-891c-413073a2db0a,
  abstract     = {{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.}},
  author       = {{Hansen, Lisbeth and Schmidt-Christensen, Anja and Gupta, Shashank and Fransén Pettersson, Nina and Hannibal, Tine and Reizis, Boris and Santamaria, Pere and Holmberg, Dan}},
  issn         = {{1932-6203}},
  language     = {{eng}},
  month        = {{12}},
  number       = {{12}},
  publisher    = {{Public Library of Science (PLoS)}},
  series       = {{PLoS ONE}},
  title        = {{E2-2 Dependent Plasmacytoid Dendritic Cells Control Autoimmune Diabetes.}},
  url          = {{http://dx.doi.org/10.1371/journal.pone.0144090}},
  doi          = {{10.1371/journal.pone.0144090}},
  volume       = {{10}},
  year         = {{2015}},
}