Journal
EUROPEAN JOURNAL OF IMMUNOLOGY
Volume 42, Issue 10, Pages 2555-2563Publisher
WILEY-BLACKWELL
DOI: 10.1002/eji.201142239
Keywords
Autoimmunity; Dendritic cells; EAE; MS; T cells; Th cells
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Funding
- The Swedish Research Council
- The Swedish Research Council Formas
- Petrus and Augusta Hedlund's Foundation
- Torn-spiran foundation
- The Hoff family (via The Swedish Brain Foundation)
- The Swedish Association for the Neurologically Disabled
- Torsten and Ragnar Soderbergs Foundation
- The Lars Hierta Memorial Foundation
- Magnus Bergvall's Foundation
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EAE, an animal model for multiple sclerosis, is a Th17- and Th1-cell-mediated auto-immune disease, but the mechanisms leading to priming of encephalitogenicTcells in autoimmune neuroinflammation are poorly understood. To investigate the role of dendritic cells (DCs) in the initiation of autoimmuneTh17- andTh1-cell responses andEAE, we used mice transgenic for a simian diphtheria toxin receptor (DTR) expressed under the control of the murineCD11c promoter (CD11c-DTRmice onC57BL/6 background).EAEwas induced by immunization with myelin oligodendrocyte glycoprotein (MOG) protein in CFA. DCs were depleted on the day before and 8 days afterMOG immunization. The mean clinicalEAEscore was only mildly reduced inDC-depleted mice when DCs were ablated beforeEAEinduction. The frequency of activatedTh cells was not altered, andMOG-inducedTh17 orTh1-cell responses were not altered, in the spleens ofDC-depleted mice. Similar results were obtained ifDCswere ablated the first 10 days afterMOGimmunization with repeatedDCdepletions. Unexpectedly, transient depletion of DCs did not affect priming or differentiation of MOG-inducedTh17 andTh1-cell responses or the incidence ofEAE. Thus, the mechansim of priming ofTh cells inEAEremains to be elucidated.
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