Chemokine Receptor CCR2 Is Not Essential for the Development of Experimental Cerebral Malaria-Reference-Cited by-同舟云学术

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

Published:2003-06 Issue:6 Volume:71 Page:3648-3651
ISSN:0019-9567
Container-title:Infection and Immunity
language:en
Short-container-title:Infect Immun

Author:

Belnoue Elodie¹,Costa Fabio T. M.¹,Vigário Ana M.¹,Voza Tatiana²,Gonnet Françoise¹²,Landau Irène²,van Rooijen Nico³,Mack Matthias⁴,Kuziel William A.⁵,Rénia Laurent¹

Affiliation:

1. Département d'Immunologie, Institut Cochin, INSERM U567, CNRS UMR 8104, Université René Descartes, Hôpital Cochin

2. Museum National d'Histoire Naturelle, Paris, France

3. Department of Cell Biology and Immunology, Faculty of Medicine, Vrije Universiteit, Amsterdam 1081 BT, The Netherlands

4. Medical Polyclinic, University of Munich, 80336 Munich, Germany

5. Department of Microbiology and Institute for Cellular and Molecular Biology, University of Texas, Austin, Texas 78712-1095

Abstract

ABSTRACT 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.

Publisher

American Society for Microbiology

Subject

Infectious Diseases,Immunology,Microbiology,Parasitology

Link

https://journals.asm.org/doi/pdf/10.1128/IAI.71.6.3648-3651.2003

Reference29 articles.

1. Amani, V., A. M. Vigario, E. Belnoue, M. Marussig, L. Fonseca, D. Mazier, and L. Rénia. 2000. Involvement of IFN-γ receptor-mediated signaling in pathology and anti-malarial immunity induced by Plasmodium berghei infection. Eur. J. Immunol.30:1646-1655.

2. Belnoue, E., M. Kayibanda, A. M. Vigario, J. C. Deschemin, N. Van Rooijen, M. Viguier, G. Snounou, and L. Renia. 2002. On the pathogenic role of brain-sequestered αβ CD8+ T cells in experimental cerebral malaria. J. Immunol.169:6369-6375.

3. Belnoue E. M. Kayibanda J.-C. Deschemin M. Viguier M. Mack W. A. Kuziel and L. Renia. CCR5 deficiency decreases susceptibility to experimental cerebral malaria. Blood in press.

4. Berendt, A. R., G. D. H. Turner, and C. I. Newbold. 1994. Cerebral malaria: the sequestration hypothesis. Parasitol. Today10:412-414.

5. Berger, O., X. Gan, C. Gujuluva, A. R. Burns, G. Sulur, M. Stins, D. Way, M. Witte, M. Weinand, J. Said, K. S. Kim, D. Taub, M. C. Graves, and M. Fiala. 1999. CXC and CC chemokine receptors on coronary and brain endothelia. Mol. Med.5:795-805.

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