Graduate Research Assistant University of Utah Salt Lake City, Utah, United States
Disclosure(s):
Ibtissam Essaghir, PhD: No financial relationships to disclose
Introduction/Rationale: 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.
