CCR2Ly-6C(hi) monocytes are crucial for the effector phase of autoimmunity in the central nervous system

Mildner, Alexander and Mack, Matthias and Schmidt, Hauke and Brueck, Wolfgang and Djukic, Marija and Zabel, Mark D. and Hille, Andrea and Priller, Josef and Prinz, Marco (2009) CCR2Ly-6C(hi) monocytes are crucial for the effector phase of autoimmunity in the central nervous system. BRAIN, 132. pp. 2487-2500. ISSN 0006-8950,

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Abstract

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. CCR2Ly-6C(hi) 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 CCR2Ly-6C(hi) monocytes during autoimmune inflammation of the central nervous system.

Item Type: Article
Uncontrolled Keywords: CHEMOKINE RECEPTOR 2; MICROVASCULAR ENDOTHELIAL-CELLS; COLLAGEN-INDUCED ARTHRITIS; MULTIPLE-SCLEROSIS; BACTERIAL-INFECTION; BONE-MARROW; CHEMOATTRACTANT PROTEIN-1; ENCEPHALOMYELITIS EAE; BRAIN MICROVESSELS; RAT-BRAIN; autoimmune encephalitis; chemokines; monocytes; multiple sclerosis
Subjects: 600 Technology > 610 Medical sciences Medicine
Divisions: Medicine > Lehrstuhl für Innere Medizin II
Depositing User: Dr. Gernot Deinzer
Date Deposited: 07 Sep 2020 13:47
Last Modified: 07 Sep 2020 13:47
URI: https://pred.uni-regensburg.de/id/eprint/28432

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