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Nat Rev Neurol. 2016 Feb;12(2):95-105. doi: 10.1038/nrneurol.2015.248. Epub 2016 Jan 18.

CCR5 blockade for neuroinflammatory diseases--beyond control of HIV.

Author information

1
Department of Infectious and Tropical Diseases, Toulouse University Hospital, Place du Docteur Baylac, TSA 40031, 31059 Toulouse cedex 9, France.
2
INSERM U1043, CNRS UMR 5282, Centre de Physiopathologie Toulouse-Purpan, Purpan Hospital, BP 3028, 31024 Toulouse cedex 3, France.
3
Department of Neurology, Pole des Neurosciences, Toulouse University Hospital, Place du Docteur Baylac TSA 40031, 31059 Toulouse cedex 9, France.
4
Center for Brain Research, Medical University of Vienna, Spitalgasse 4, A-1090 Vienna, Austria.

Abstract

Chemokine receptors have been implicated in a wide range of CNS inflammatory diseases and have important roles in the recruitment and positioning of immune cells within tissues. Among them, the chemokine (C-C motif) receptor 5 (CCR5) can be targeted by maraviroc, a readily available and well-tolerated drug that was developed for the treatment of HIV. Correlative evidence implicates the CCR5-chemokine axis in multiple sclerosis, Rasmussen encephalitis, progressive multifocal leukoencephalopathy-associated immune reconstitution inflammatory syndrome, and infectious diseases, such as cerebral malaria and HIV-associated neurocognitive disorders. On the basis of this evidence, we postulate in this Review that CCR5 antagonists, such as maraviroc, offer neuroprotective benefits in settings in which CCR5 promotes deleterious neuroinflammation, particularly in diseases in which CD8(+) T cells seem to play a pivotal role.

PMID:
26782333
DOI:
10.1038/nrneurol.2015.248
[Indexed for MEDLINE]

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