BACKGROUND: Accumulating evidence supports a major role of B cells in multiple 
sclerosis (MS) pathogenesis. How B cells are recruited to the CNS is 
incompletely understood. Our objective was to study B-cell chemokine 
concentrations in MS, their relationship with disease activity, and how 
treatment with methylprednisolone and natalizumab affected the concentration in 
CSF.
METHODS: Using a cross-sectional design, CSF and blood samples were obtained 
from cohorts of patients with clinically isolated syndromes (CIS), 
relapsing-remitting MS (RRMS), primary progressive MS (PPMS), or secondary 
progressive MS (SPMS), and noninflammatory neurologic disease control subjects. 
Some patients with RRMS were studied before and after treatment with 
methylprednisolone or natalizumab.
RESULTS: In CSF, concentrations of CXCL13, but not CXCL12, were higher in 
patients with CIS, RRMS, SPMS, and PPMS than in controls. CSF concentrations of 
CXCL13 correlated with the CSF B-cell count, with markers of immune activation, 
and with disease activity in patients with CIS and RRMS. CSF concentrations of 
CXCL13 decreased after treatment with high-dose methylprednisolone and 
natalizumab. High CSF concentrations of CXCL13 correlated with low expression of 
messenger RNA encoding the immunoregulatory cytokines interleukin 10 and 
transforming growth factor beta1, but not with the expression of T-helper type 1 
(Th1) and Th17 factors.
CONCLUSION: The chemokine CXCL13 may play a major role in recruitment of B cells 
and T-cell subsets expressing the chemokine receptor CXCR5 to the CNS in 
multiple sclerosis (MS), and may be a useful biomarker for treatment effects in 
MS. Furthermore, CXCL13 or its receptor CXCR5 should be considered as 
therapeutic targets in MS.