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Infection and Immunity, June 2003, p. 3648-3651, Vol. 71, No. 6
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.6.3648-3651.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Chemokine Receptor CCR2 Is Not Essential for the Development of Experimental Cerebral Malaria

Elodie Belnoue,1 Fabio T. M. Costa,1 Ana M. Vigário,1 Tatiana Voza,2 Françoise Gonnet,1,2 Irène Landau,2 Nico van Rooijen,3 Matthias Mack,4 William A. Kuziel,5 and Laurent Rénia1*

Département d'Immunologie, Institut Cochin, INSERM U567, CNRS UMR 8104, Université René Descartes, Hôpital Cochin,1 Museum National d'Histoire Naturelle, Paris, France,2 Department of Cell Biology and Immunology, Faculty of Medicine, Vrije Universiteit, Amsterdam 1081 BT, The Netherlands,3 Medical Polyclinic, University of Munich, 80336 Munich, Germany,4 Department of Microbiology and Institute for Cellular and Molecular Biology, University of Texas, Austin, Texas 78712-10955

Received 13 January 2003/ Returned for modification 14 February 2003/ Accepted 6 March 2003

Infection with Plasmodium berghei ANKA induces cerebral malaria in susceptible mice. Brain-sequestered CD8+ T cells are responsible for this pathology. We have evaluated the role of CCR2, a chemokine receptor expressed on CD8+ T cells. Infected CCR2-deficient mice were as susceptible to cerebral malaria as wild-type mice were, and CD8+ T-cell migration to the brain was not abolished.

* Corresponding author. Mailing address: Département d'Immunologie, Institut Cochin, Hôpital Cochin, BÂtiment Gustave Roussy, 27 rue du Fbg St Jacques, 75014 Paris, France. Phone: 33 1 40 51 65 11. Fax: 33 1 40 51 65 35. E-mail: renia{at}cochin.inserm.fr.

Editor: W. A. Petri, Jr.

Infection and Immunity, June 2003, p. 3648-3651, Vol. 71, No. 6
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.6.3648-3651.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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