| First Author | Harris VK | Year | 2017 |
| Journal | PLoS One | Volume | 12 |
| Issue | 4 | Pages | e0175575 |
| PubMed ID | 28388685 | Mgi Jnum | J:248560 |
| Mgi Id | MGI:5918075 | Doi | 10.1371/journal.pone.0175575 |
| Citation | Harris VK, et al. (2017) Fetuin-A deficiency protects mice from Experimental Autoimmune Encephalomyelitis (EAE) and correlates with altered innate immune response. PLoS One 12(4):e0175575 |
| abstractText | 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-1beta 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. |
