tetano
Editor, Senior Moderator
J Virol. 2012 Jan 25. [Epub ahead of print]
Tissue exit - a novel control point in the accumulation of antigen-specific CD8 T cells in the influenza A virus-infected lung.
Jennrich S, Lee MH, Lynn RC, Dewberry K, Debes GF.
Source
Department of Pathobiology.
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.
PMID:
22278253
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/22278253
Tissue exit - a novel control point in the accumulation of antigen-specific CD8 T cells in the influenza A virus-infected lung.
Jennrich S, Lee MH, Lynn RC, Dewberry K, Debes GF.
Source
Department of Pathobiology.
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.
PMID:
22278253
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/22278253