tetano
Editor, Senior Moderator
J Virol. 2011 Dec 28. [Epub ahead of print]
Influenza A Virus Infection Results in a Robust, Antigen-Responsive and Widely Disseminated Foxp3+ Regulatory T Cell Response.
Betts RJ, Prabhu N, Ho AW, Lew FC, Hutchinson PE, Rotzschke O, Macary PA, Kemeny DM.
Source
Department of Microbiology, Immunology Programme, National University of Singapore, Singapore, 117597.
Abstract
Foxp3(+)CD4(+) regulatory T cells represent a highly suppressive T cell subset with well-characterized immunosuppressive effects during immune homeostasis and chronic infections, although the role of these cells in acute viral infections is poorly understood. The present study sought to examine the induction of Foxp3(+)CD4(+) Treg cells in a non-lethal murine model of pulmonary viral infection using the prototypical respiratory virus influenza A. We establish that influenza A virus infection results in a robust Foxp3(+)CD4(+) T cell response, and that regulatory T cell induction at the site of inflammation precedes that of the effector T cell response. Induced Foxp3(+)CD4(+) T cells are highly suppressive ex vivo, demonstrating influenza-induced Foxp3(+)CD4(+) T cells are phenotypically regulatory T cells. Influenza A virus-induced regulatory T cells proliferate vigorously in response to influenza antigen, are disseminated throughout the site of infection and primary and secondary lymphoid organs and retain Foxp3 expression in vitro, suggesting acute viral infection is capable of inducing a foreign-antigen specific Treg response. The ability of influenza-induced regulatory T cells to suppress antigen-specific CD4(+) and CD8(+) T cell proliferation and cytokine production correlates closely to their ability to respond to influenza antigens, suggesting virus-induced Treg cells are capable of attenuating effector responses in an antigen-dependent manner. Collectively these data demonstrate primary acute viral infection is capable of inducing a robust, antigen-responsive and suppressive regulatory T cell response.
PMID:
22205730
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/22205730
Influenza A Virus Infection Results in a Robust, Antigen-Responsive and Widely Disseminated Foxp3+ Regulatory T Cell Response.
Betts RJ, Prabhu N, Ho AW, Lew FC, Hutchinson PE, Rotzschke O, Macary PA, Kemeny DM.
Source
Department of Microbiology, Immunology Programme, National University of Singapore, Singapore, 117597.
Abstract
Foxp3(+)CD4(+) regulatory T cells represent a highly suppressive T cell subset with well-characterized immunosuppressive effects during immune homeostasis and chronic infections, although the role of these cells in acute viral infections is poorly understood. The present study sought to examine the induction of Foxp3(+)CD4(+) Treg cells in a non-lethal murine model of pulmonary viral infection using the prototypical respiratory virus influenza A. We establish that influenza A virus infection results in a robust Foxp3(+)CD4(+) T cell response, and that regulatory T cell induction at the site of inflammation precedes that of the effector T cell response. Induced Foxp3(+)CD4(+) T cells are highly suppressive ex vivo, demonstrating influenza-induced Foxp3(+)CD4(+) T cells are phenotypically regulatory T cells. Influenza A virus-induced regulatory T cells proliferate vigorously in response to influenza antigen, are disseminated throughout the site of infection and primary and secondary lymphoid organs and retain Foxp3 expression in vitro, suggesting acute viral infection is capable of inducing a foreign-antigen specific Treg response. The ability of influenza-induced regulatory T cells to suppress antigen-specific CD4(+) and CD8(+) T cell proliferation and cytokine production correlates closely to their ability to respond to influenza antigens, suggesting virus-induced Treg cells are capable of attenuating effector responses in an antigen-dependent manner. Collectively these data demonstrate primary acute viral infection is capable of inducing a robust, antigen-responsive and suppressive regulatory T cell response.
PMID:
22205730
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/22205730