Fetuin-A deficiency protects mice from Experimental Autoimmune Encephalomyelitis

Fetuin-A is a biomarker of disease activity in multiple sclerosis. Our aim was to investigate whether Fetuin-A plays a direct role in the neuroinflammatory response in the mouse EAE model. Peak Fetuin-A expression in the CNS and in peripheral lymphoid tissue correlated with peak EAE disease activity...

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Bibliographic Details
Published inPloS one Vol. 12; no. 4; p. e0175575
Main Authors Harris, Violaine K, Bell, Lena, Langan, Ruth-Anne, Tuddenham, John, Landy, Mark, Sadiq, Saud A
Format Journal Article
LanguageEnglish
Published Public Library of Science 07.04.2017
Subjects
Alpha fetoproteins
Encephalomyelitis
Health aspects
Immune response
Prevention
Risk factors
United States
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Summary:Fetuin-A is a biomarker of disease activity in multiple sclerosis. Our aim was to investigate whether Fetuin-A plays a direct role in the neuroinflammatory response in the mouse EAE model. Peak Fetuin-A expression in the CNS and in peripheral lymphoid tissue correlated with peak EAE disease activity. Fetuin-A-deficient mice showed reduced EAE severity associated with an accumulation of splenic monocyte and dendritic cell populations, increased IL-12p40, ASC1, and IL-1[beta] expression, and an increase in T regulatory cells. The upregulation of Fetuin-A in LPS-stimulated dendritic cells and microglia further supports an intrinsic role of Fetuin-A in regulating innate immune activation during EAE.
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0175575