To further characterize these ectopic structures and explore the mechanisms allowing for the establishment of a permissive microenvironment for the virus persistence, we tested the hypothesis that, similarly to B follicles in secondary lymphoid tissues, FDC express/upregulate PD-L1 and interact with intrafollicular CD4+ T cells expressing PD-1 within meningeal TLSs in MS. This evidence concerns the gene CD274 and myeloid sarcoma.