Figure 1.

B cell antigen presentation in MS. B cells could contribute to the activation of pathogenic T cells through presentation of self and non-self antigens. (A) CD27+ CD20+ memory B cells could present self-peptides from proteins that are expressed in the CNS leading to the induction of autoreactive T cells. Infection of B cells with EBV induces EBV-specific T cells that exert continuous immune surveillance and are essential for virus-host homeostasis. EBV infected B cells could induce autoreactive T cells by presenting EBV peptides sharing similarities with peptides from CNS self-antigens (i.e. MBP, RASGPR2) (molecular mimicry). Autoreactive T cells homing to the CNS would recognize their target antigen on local antigen presenting cells (APC) and become reactivated causing CNS inflammation and tissue injury. (B) EBV infected CD27+ CD20+ memory B cells induce EBV-specific T cells that migrate in the CNS to counteract an abnormal EBV infection brought inside the CNS by circulating infected B cells. In this model, B cells would act as APC both in the periphery and in the CNS to stimulate a detrimental antiviral immune response causing CNS inflammation and tissue injury.