Suppression of Experimental Autoimmune Encephalomyelitis by ILT3.Fc

• DOI: 10.4049/jimmunol.2000265
• Publication Date: 2020-12-23T21:32:54Z
• Authors: Zheng Xu; Chun-Chieh Lin; Sophey Ho; George Vlad; Nicole Suciu-Foca
• Keywords: Encephalomyelitis

Abstract Multiple sclerosis (MS) is a chronic autoimmune disease of the CNS that characterized by demyelination, axonal loss, gliosis, and inflammation. The murine model MS experimental encephalopathy (EAE) induced immunization mice with myelin oligodendrocyte glycoprotein (MOG)35–55. Ig-like transcript 3 (ILT3) an inhibitory cell surface receptor expressed tolerogenic human dendritic cells. In this study, we show recombinant ILT3.Fc protein binds to immune cells inhibits release proinflammatory cytokines cause neuroinflammatory process result in paralysis. Administration prevents rapid evolution C57BL/6 associated profound reduction proliferation MOG35–55–specific Th1 Th17 Inhibition IFN-γ IL-17A treated delayed time onset its peak clinical score. Neuropathological analysis shows inflammatory infiltrates demyelinated areas brains spinal cords mice. These results indicate inhibition development provides effective suppression EAE suggests feasibility approach based on use for treatment MS. Furthermore, our open way further studies effect models autoimmunity cancer.