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Brain Advance Access originally published online on June 16, 2009
Brain 2009 132(9):2487-2500; doi:10.1093/brain/awp144
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© The Author (2009). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

CCR2+Ly-6Chi monocytes are crucial for the effector phase of autoimmunity in the central nervous system

Alexander Mildner1, Matthias Mack2, Hauke Schmidt3, Wolfgang Brück3, Marija Djukic4, Mark D. Zabel5, Andrea Hille6, Josef Priller7 and Marco Prinz1

1 Department of Neuropathology, University of Freiburg, Freiburg, Germany 2 Department of Internal Medicine, University of Regensburg, Regensburg, Germany 3 Department of Neuropathology, Georg-August University, Göttingen, Germany 4 Department of Neurology, Georg-August University, Göttingen, Germany 5 Department of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins, Colorado, USA 6 Department of Radiation Oncology, Georg-August University, Göttingen, Germany 7 Neuropsychiatry and Laboratory of Molecular Psychiatry, Charité-Universitätsmedizin Berlin, Berlin, Germany

Correspondence to: Marco Prinz, MD, Department of Neuropathology, University of Freiburg, Breisacher Str. 64, D-79106 Freiburg, Germany E-mail: marco.prinz{at}uniklinik-freiburg.de

The chemokine receptor CCR2 plays a vital role for the induction of autoimmunity in the central nervous system. However, it remains unclear how the pathogenic response is mediated by CCR2-bearing cells. By combining bone marrow chimerism with gene targeting we detected a mild disease-modulating role of CCR2 during experimental autoimmune encephalomyelitis, a model for central nervous system autoimmunity, on radio-resistant cells that was independent from targeted CCR2 expression on endothelia. Interestingly, absence of CCR2 on lymphocytes did not influence autoimmune demyelination. In contrast, engagement of CCR2 on accessory cells was required for experimental autoimmune encephalomyelitis induction. CCR2+Ly-6Chi monocytes were rapidly recruited to the inflamed central nervous system and were crucial for the effector phase of disease. Selective depletion of this specific monocyte subpopulation through engagement of CCR2 strongly reduced central nervous system autoimmunity. Collectively, these data indicate a disease-promoting role of CCR2+Ly-6Chi monocytes during autoimmune inflammation of the central nervous system.

Key Words: autoimmune encephalitis; chemokines; monocytes; multiple sclerosis

Received December 10, 2008. Revised March 25, 2009. Accepted April 24, 2009.


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