Affiliations: Department of Neurology, University of Michigan Medical School, Ann Arbor, MI, USA
Correspondence:
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Correspondence to: Dr. David Irani, Department of Neurology, University of Michigan Medical School, 4007 Biomedical Sciences Research Building, 109 Zina Pitcher Place, Ann Arbor, MI 40109-2200, USA. Tel.: +1 734 615 5635; Fax: +1 734 615 7300; E-mail: [email protected]
Abstract: The chemokine, C-X-C motif ligand 13 (CXCL13), is constitutively expressed in lymphoid organs and controls the recruitment and compartmentalization of lymphocytes and antigen presenting cells within these specialized structures. Recent data, however, also find induction of this molecule during central nervous system (CNS) inflammation under a variety of circumstances. While its role(s) in the pathogenesis of neoplastic, infectious and autoimmune disorders of the CNS remain incompletely understood, several lines of evidence suggest that CXCL13 could become a relevant therapeutic target in at least some of these diseases. This review focuses on how CXCL13 contributes to the pathogenesis of selected CNS disorders involving both experimental animals and humans, paying particular attention to the issue of whether (and if so, how) blockade of this ligand or its receptor might benefit the host. Current blocking strategies largely involve the use of monoclonal antibodies, but an improved understanding of downstream signaling pathways makes small molecule inhibition a future possibility.
Keywords: CXCL13, lymphoid chemokines, CXCR5, neuroborreliosis, primary central nervous system lymphoma, multiple sclerosis, post-stroke dementia
