Abstract:
:Apolipoprotein E (ApoE) functions as a ligand in receptor-mediated endocytosis of lipoprotein particles and has been demonstrated to play a role in antigen presentation. To explore the contribution of ApoE during autoimmune central nervous system (CNS) demyelination, we examined the clinical, cellular immune function, and pathologic consequences of experimental autoimmune encephalomyelitis (EAE) induction in ApoE knockout (ApoE(-/-)) mice. We observed reduced clinical severity of EAE in ApoE(-/-) mice in comparison to WT mice that was concomitant with an early reduction of dendritic cells (DCs) followed by a reduction of additional innate cells in the spinal cord at the peak of disease without any differences in axonal damage. While T cell priming was enhanced in ApoE(-/-) mice, reduced severity of EAE was also observed in ApoE(-/-) recipients of encephalitogenic wild type T cells. Expression of ApoE during EAE was elevated within the CNS of wild type mice, particularly by innate cells such as DCs. Overall, ApoE promotes clinical EAE, likely by mediation of inflammation localized within the CNS.
journal_name
J Neuroimmunoljournal_title
Journal of neuroimmunologyauthors
Shin S,Walz KA,Archambault AS,Sim J,Bollman BP,Koenigsknecht-Talboo J,Cross AH,Holtzman DM,Wu GFdoi
10.1016/j.jneuroim.2014.03.010subject
Has Abstractpub_date
2014-06-15 00:00:00pages
8-17issue
1-2eissn
0165-5728issn
1872-8421pii
S0165-5728(14)00074-5journal_volume
271pub_type
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