CX3CL1 (fractalkine) and CX3CR1 expression in myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis: kinetics and cellular origin |
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| Authors: | Dan Sunnemark Sana Eltayeb Maria Nilsson Erik Wallstr?m Hans Lassmann Tomas Olsson Anna-Lena Berg and Anders Ericsson-Dahlstrand |
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| Institution: | (1) Department of Molecular Sciences, AstraZeneca R&D S?dert?lje, S-151 85 S?dert?lje, Sweden;(2) Neuroimmunology Unit, Department of Clinical Neuroscience, Karolinska Institutet, S-171 76 Stockholm, Sweden;(3) Neurological Institute, University of Vienna, Austria;(4) Safety Assessment, AstraZeneca R&D S?dert?lje, S-151 85 S?dert?lje, Sweden |
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| Abstract: | Background Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS). It is associated with local
activation of microglia and astroglia, infiltration of activated macrophages and T cells, active degradation of myelin and
damage to axons and neurons. The proposed role for CX3CL1 (fractalkine) in the control of microglia activation and leukocyte infiltration places this chemokine and its receptor
CX3CR1 in a potentially strategic position to control key aspects in the pathological events that are associated with development
of brain lesions in MS. In this study, we examine this hypothesis by analyzing the distribution, kinetics, regulation and
cellular origin of CX3CL1 and CX3CR1 mRNA expression in the CNS of rats with an experimentally induced MS-like disease, myelin oligodendrocyte glycoprotein
(MOG)-induced autoimmune encephalomyelitis (EAE). |
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