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Exploring the Role of CCR6/CCL20 Axis in B Cell Migration into the CNS during EAE

B cells have been implicated in the pathogenesis of multiple sclerosis (MS) but how they migrate into the central nervous system (CNS) is poorly understood. Previous work demonstrated the use of chemokine CCL20 signaling through CCR6, in driving B cell migration during various states of inflammation. Using a transwell assay, we determined that CCR6 expressing B cells are responsive to CCL20 in a dose-dependent manner. During experimental autoimmune encephalomyelitis (EAE), CCR6 expression is upregulated on CNS-infiltrated B cells and there is increased serum concentration of CCL20. However, lack of CCR6 expression on B cells did not affect their ability to migrate into the CNS nor did it affect the severity of disease in a B cell independent model of EAE. Our data therefore suggest that the CCR6/CCL20 axis is not the main driver of B cell migration into the CNS during EAE.