Temporal expression and cellular origin of CC chemokine receptors CCR1, CCR2 and CCR5 in the central nervous system: insight into mechanisms of MOG-induced EAE |
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| Authors: | Sana Eltayeb Anna-Lena Berg Hans Lassmann Erik Wallström Maria Nilsson Tomas Olsson Anders Ericsson-Dahlstrand Dan Sunnemark |
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| Affiliation: | (1) Department of Clinical Neuroscience, Center for Molecular Medicine, Neuroimmunology Unit, Karolinska Institute, S-171 76 Stockholm, Sweden;(2) Department of Pathology, Safety Assessment, AstraZeneca R&D Sdertlje, S-15185 Sdertlje, Sweden;(3) Brain Research Institute, University of Vienna, Vienna, Austria;(4) Department of Disease Biology, Local Discovery Research Area CNS and Pain Control, AstraZeneca R&D Sdertlje, S-151 85 Sdertlje, Sweden |
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| Abstract: | ![]()
Background The CC chemokine receptors CCR1, CCR2 and CCR5 are critical for the recruitment of mononuclear phagocytes to the central nervous system (CNS) in multiple sclerosis (MS) and other neuroinflammatory diseases. Mononuclear phagocytes are effector cells capable of phagocytosing myelin and damaging axons. In this study, we characterize the regional, temporal and cellular expression of CCR1, CCR2 and CCR5 mRNA in the spinal cord of rats with myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis (MOG-EAE). While resembling human MS, this animal model allows unique access to CNS-tissue from various time-points of relapsing neuroinflammation and from various lesional stages: early active, late active, and inactive completely demyelinated lesions. |
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