Viral (LCMV) coinfection decreases the number of pathogenic Th17 cells in the CNS and prevents demyelinating disease 2309860

Introduction Multiple sclerosis is a chronic autoimmune demyelinating disease impacting 2.9 million people worldwide. Despite the significant advances in understanding the pathogenicity of CD4+ T cells, there is no cure. Infections have often been considered a trigger for the development of autoimmune diseases, yet infections can also have potential protective roles. Here, we investigate the impact of viral co-infection on demyelinating disease. Methods We found that infecting C57Bl/6 mice with lymphocytic choriomeningitis virus (LCMV) during experimental autoimmune encephalomyelitis (EAE) leads to complete protection from demyelinating disease onset and progressive paralysis compared to uninfected controls. Results Overall, there was a substantial decrease in the numbers of pathogenic Th17 CD4 T cells. Using 2D-micropipette adhesion frequency assay, we demonstrated reduction in the overall number of myelin specific T cells and their affinity for MOG35-55. In adoptive transfer experiments, LCMV infection also prevented demyelinating disease induced by 2D2 TCR Tg CD4+ T cells. While viral coinfection prevented disease, Type I interferon was not the causative mechanism. Conclusion Our work indicates that viral co-infection can decrease the number and affinity of pathogenic, myelin specific CD4 T cells in the CNS.