Chemokine receptor CCR2 is not essential for the development of experimental cerebral malaria

被引：33

作者：

Belnoue, E

Costa, FTM

Vigário, AM

Voza, T

Gonnet, F

Landau, I

van Rooijen, N

Mack, M

Kuziel, WA

Rénia, L

机构：

[1] Univ Paris 05, CNRS UMR 8104,Hop Cochin, INSERM U567,Inst Cochin Genet Mol, Dept Immunol, F-75014 Paris, France

[2] Museum Natl Hist Nat, F-75231 Paris, France

[3] Vrije Univ Amsterdam, Fac Med, Dept Cell Biol & Immunol, NL-1081 BT Amsterdam, Netherlands

[4] Univ Munich, Med Policlin, D-80336 Munich, Germany

[5] Univ Texas, Dept Microbiol, Austin, TX 78712 USA

[6] Univ Texas, Inst Cellular & Mol Biol, Austin, TX 78712 USA

来源：

INFECTION AND IMMUNITY | 2003年 / 71卷 / 06期

关键词：

D O I：

10.1128/IAI.71.6.3648-3651.2003

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

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.

引用

页码：3648 / 3651

页数：4

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