Fetuin-A deficiency protects mice from Experimental Autoimmune Encephalomyelitis (EAE) and correlates with altered innate immune response.
Violaine K HarrisLena BellRuth-Anne LanganJohn TuddenhamMark LandySaud A SadiqPublished in: PloS one (2017)
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-1β 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.
Keyphrases
- dendritic cells
- disease activity
- immune response
- systemic lupus erythematosus
- rheumatoid arthritis
- rheumatoid arthritis patients
- poor prognosis
- ankylosing spondylitis
- multiple sclerosis
- regulatory t cells
- juvenile idiopathic arthritis
- innate immune
- inflammatory response
- induced apoptosis
- transcription factor
- long non coding rna
- toll like receptor
- signaling pathway
- spinal cord injury
- endoplasmic reticulum stress
- oxidative stress
- skeletal muscle
- neuropathic pain
- genetic diversity
- nlrp inflammasome