IFN-Inducible Protein 10/CXC Chemokine Ligand 10-Independent Induction of Experimental Autoimmune Encephalomyelitis

摘要: In multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE), autoaggressive T cells traffic into the CNS induce disease. Infiltration of these pathogenic has been correlated with expression chemokine IFN-inducible protein (IP)10/CXC ligand (CXCL)10, a chemoattractant for activated cells, receptor CXCR3, in both MS patients mice EAE. present study, we report that targeted deletion IP-10 did not diminish expression, severity, or histopathology EAE induced by active immunization 100 μg myelin oligodendrocyte glycoprotein peptide (MOG)p35–55. However, found IP-10-deficient had lower threshold disease compared wild-type littermates. 5 MOGp35–55 resulted more severe characterized greater number lesions infiltrating mononuclear controls. immunized demonstrated increased levels cell α-chemokine/CXCL11 mRNA decreased monokine IFN-γ/CXCL9 draining lymph nodes, suggesting differential compensation loss lymphoid vs parenchymal tissue compartments. low-dose was associated enhanced Ag-specific Th1 responses node, which corresponded diminished node TGF-β1 expression. Our data required trafficking but played an unexpected role determining susceptibility periphery.