Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
3065401 | Journal of Neuroimmunology | 2008 | 11 Pages |
Abstract
Prion diseases are neurodegenerative infections with gliosis and vacuolation. The mechanisms of degeneration remain unclear, but chemokines may be important. In current experiments CCR1 knock-out (KO) mice succumbed more rapidly to scrapie infection than WT controls. Infected KO mice had upregulation of CCL3, a CCR1 ligand, and CCR5, a receptor with specificity for CCL3. Both infected KO and WT mice had upregulation of CCR5-mediated signaling involving activation of Erk1/2 in astrocytes; however, activation was earlier in KO mice suggesting a role in pathogenesis. In both mouse strains activation of the Erk1/2 pathway may lead to astrocyte dysfunction resulting in neurodegeneration.
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Authors
Rachel A. LaCasse, James F. Striebel, Cynthia Favara, Lisa Kercher, Bruce Chesebro,