Protective capacity and epitope specificity of CD8+ T cells responding to lethal West Nile virus infection

2007 ◽  
Vol 37 (7) ◽  
pp. 1855-1863 ◽  
Author(s):  
James D. Brien ◽  
Jennifer L. Uhrlaub ◽  
Janko Nikolich-Žugich
Keyword(s):  
T Cells ◽  
West Nile Virus ◽  
Virus Infection ◽  
Cd8 T Cells ◽  
West Nile Virus Infection ◽  
Protective Capacity ◽  
West Nile ◽  
Epitope Specificity

scholarly journals Increased Frequency of Tim-3 Expressing T Cells Is Associated with Symptomatic West Nile Virus Infection

PLoS ONE ◽  
2014 ◽  
Vol 9 (3) ◽  
pp. e92134 ◽  
Author(s):  
Marion C. Lanteri ◽  
Michael S. Diamond ◽  
Jacqueline P. Law ◽  
Glen M. Chew ◽  
Shiquan Wu ◽  
...  
Keyword(s):  
T Cells ◽  
West Nile Virus ◽  
Virus Infection ◽  
West Nile Virus Infection ◽  
West Nile

scholarly journals IFN-γ-Producing γδ T Cells Help Control Murine West Nile Virus Infection

2003 ◽  
Vol 171 (5) ◽  
pp. 2524-2531 ◽  
Author(s):  
Tian Wang ◽  
Eileen Scully ◽  
Zhinan Yin ◽  
Jung H. Kim ◽  
Sha Wang ◽  
...  
Keyword(s):  
T Cells ◽  
West Nile Virus ◽  
Virus Infection ◽  
Γδ T Cells ◽  
West Nile Virus Infection ◽  
West Nile ◽  
Ifn Γ

scholarly journals Vγ4+T cells regulate host immune response to West Nile virus infection

2011 ◽  
Vol 63 (2) ◽  
pp. 183-192 ◽  
Author(s):  
Thomas Welte ◽  
Judith Aronson ◽  
Bin Gong ◽  
Aparna Rachamallu ◽  
Nicole Mendell ◽  
...  
Keyword(s):  
Immune Response ◽  
T Cells ◽  
West Nile Virus ◽  
Virus Infection ◽  
West Nile Virus Infection ◽  
Host Immune Response ◽  
West Nile

scholarly journals γδd T cells promote the maturation of dendritic cells during West Nile virus infection

2010 ◽  
Vol 59 (1) ◽  
pp. 71-80 ◽  
Author(s):  
Hao Fang ◽  
Thomas Welte ◽  
Xin Zheng ◽  
Gwong-Jen J. Chang ◽  
Michael R. Holbrook ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
West Nile Virus ◽  
Virus Infection ◽  
West Nile Virus Infection ◽  
West Nile

scholarly journals γδ T Cells Facilitate Adaptive Immunity against West Nile Virus Infection in Mice

2006 ◽  
Vol 177 (3) ◽  
pp. 1825-1832 ◽  
Author(s):  
Tian Wang ◽  
Yunfei Gao ◽  
Eileen Scully ◽  
C. Todd Davis ◽  
John F. Anderson ◽  
...  
Keyword(s):  
T Cells ◽  
West Nile Virus ◽  
Virus Infection ◽  
Adaptive Immunity ◽  
Γδ T Cells ◽  
West Nile Virus Infection ◽  
West Nile

scholarly journals Chemokine receptor CCR5 promotes leukocyte trafficking to the brain and survival in West Nile virus infection

2005 ◽  
Vol 202 (8) ◽  
pp. 1087-1098 ◽  
Author(s):  
William G. Glass ◽  
Jean K. Lim ◽  
Rushina Cholera ◽  
Alexander G. Pletnev ◽  
Ji-Liang Gao ◽  
...  
Keyword(s):  
T Cells ◽  
West Nile Virus ◽  
Chemokine Receptor ◽  
Cd8 T Cells ◽  
West Nile Virus Infection ◽  
West Nile ◽  
Leukocyte Accumulation ◽  
Chemokine Receptor Ccr5 ◽  
The Brain ◽  
Receptor Ccr5

The molecular immunopathogenesis of West Nile virus (WNV) infection is poorly understood. Here, we characterize a mouse model for WNV using a subcutaneous route of infection and delineate leukocyte subsets and immunoregulatory factors present in the brains of infected mice. Central nervous system (CNS) expression of the chemokine receptor CCR5 and its ligand CCL5 was prominently up-regulated by WNV, and this was associated with CNS infiltration of CD4+ and CD8+ T cells, NK1.1+ cells and macrophages expressing the receptor. The significance of CCR5 in pathogenesis was established by mortality studies in which infection of CCR5−/− mice was rapidly and uniformly fatal. In the brain, WNV-infected CCR5−/− mice had increased viral burden but markedly reduced NK1.1+ cells, macrophages, and CD4+ and CD8+ T cells compared with WNV-infected CCR5+/+ mice. Adoptive transfer of splenocytes from WNV-infected CCR5+/+ mice into infected CCR5−/− mice increased leukocyte accumulation in the CNS compared with transfer of splenocytes from infected CCR5−/− mice into infected CCR5−/− mice, and increased survival to 60%, the same as in infected CCR5+/+ control mice. We conclude that CCR5 is a critical antiviral and survival determinant in WNV infection of mice that acts by regulating trafficking of leukocytes to the infected brain.

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