tetano
Editor, Senior Moderator
First published January 2012, doi: 10.1128/JVI.07025-11 J. Virol. April 2012 vol. 86 no. 7 3436-3445
Tissue Exit: a Novel Control Point in the Accumulation of Antigen-Specific CD8 T Cells in the Influenza A Virus-Infected Lung
Silke Jennricha,
Michael H. Leea,
Rachel C. Lynna,b,
Kristofer Dewberrya,c,* and
Gudrun F. Debesa
+ Author Affiliations
aDepartment of Pathobiology
bDepartment of Obstetrics and Gynecology, University of Pennsylvania, Philadelphia, Pennsylvania, USA
cDepartment of Food and Animal Sciences, University of Delaware, Newark, Delaware, USA
ABSTRACT
Memory/effector T cells efficiently migrate into extralymphoid tissues and sites of infection, providing immunosurveillance and a first line of defense against invading pathogens. Even though it is a potential means to regulate the size, quality, and duration of a tissue infiltrate, T cell egress from infected tissues is poorly understood. Using a mouse model of influenza A virus infection, we found that CD8 effector T cells egressed from the infected lung in a CCR7-dependent manner. In contrast, following antigen recognition, effector CD8 T cell egress decreased and CCR7 function was reduced in vivo and in vitro, indicating that the exit of CD8 T cells from infected tissues is tightly regulated. Our data suggest that the regulation of T cell egress is a mechanism to retain antigen-specific effectors at the site of infection to promote viral clearance, while decreasing the numbers of bystander T cells and preventing overt inflammation.
http://jvi.asm.org/content/86/7/3436.short?rss=1
Tissue Exit: a Novel Control Point in the Accumulation of Antigen-Specific CD8 T Cells in the Influenza A Virus-Infected Lung
Silke Jennricha,
Michael H. Leea,
Rachel C. Lynna,b,
Kristofer Dewberrya,c,* and
Gudrun F. Debesa
+ Author Affiliations
aDepartment of Pathobiology
bDepartment of Obstetrics and Gynecology, University of Pennsylvania, Philadelphia, Pennsylvania, USA
cDepartment of Food and Animal Sciences, University of Delaware, Newark, Delaware, USA
ABSTRACT
Memory/effector T cells efficiently migrate into extralymphoid tissues and sites of infection, providing immunosurveillance and a first line of defense against invading pathogens. Even though it is a potential means to regulate the size, quality, and duration of a tissue infiltrate, T cell egress from infected tissues is poorly understood. Using a mouse model of influenza A virus infection, we found that CD8 effector T cells egressed from the infected lung in a CCR7-dependent manner. In contrast, following antigen recognition, effector CD8 T cell egress decreased and CCR7 function was reduced in vivo and in vitro, indicating that the exit of CD8 T cells from infected tissues is tightly regulated. Our data suggest that the regulation of T cell egress is a mechanism to retain antigen-specific effectors at the site of infection to promote viral clearance, while decreasing the numbers of bystander T cells and preventing overt inflammation.
http://jvi.asm.org/content/86/7/3436.short?rss=1