J Neuroimmunol. 2004 Mar;148(1-2):11-23
Magliozzi R, Columba-Cabezas S, Serafini B, Aloisi F.
Neurophysiology Unit, Laboratory Organ, System Pathophysiology, Department of Cell Biology and Neuroscience, Istituto Superiore di Sanita, Viale Regina Elena 299, 00161 Roma, Italy.
Given the abnormalities in B-cell activity occurring in the central nervous system (CNS) of patients with multiple sclerosis (MS), we have explored the possibility that CNS inflammation induced in mouse models of experimental autoimmune encephalomyelitis (EAE) triggers expression of molecules that control the development and functional organization of lymphoid follicles, the sites where B-cell responses are initiated.
By reverse transcription-polymerase chain reaction (RT-PCR), we find that gene expression of CXCL13, a chemokine involved in B-cell recruitment into lymphoid follicles, and BAFF, a key regulator of B-cell survival, is markedly and persistently upregulated in the CNS of mice with relapsing-remitting and chronic-relapsing EAE.
Using immunohistochemical techniques, we also show the presence of lymphoid follicle-like structures containing B cells and a reticulum of CXCL13(+) and FDC-M1(+) follicular dendritic cells within the meninges of several mice undergoing progressive relapsing EAE.
These observations indicate that, under chronic inflammatory conditions, the less immunoprivileged meningeal compartment is the site where ectopic lymphoid follicles preferentially develop and where pathogenic B-cell responses could be sustained in autoimmune disorders of the CNS.