tetano
Editor, Senior Moderator
PLoS One. 2012;7(5):e37539. Epub 2012 May 18.
IL-15 Participates in the Respiratory Innate Immune Response to Influenza Virus Infection.
Verbist KC, Rose DL, Cole CJ, Field MB, Klonowski KD.
Source
Department of Cellular Biology, University of Georgia, Athens, Georgia, United States of America.
Abstract
Following influenza infection, natural killer (NK) cells function as interim effectors by suppressing viral replication until CD8 T cells are activated, proliferate, and are mobilized within the respiratory tract. Thus, NK cells are an important first line of defense against influenza virus. Here, in a murine model of influenza, we show that virally-induced IL-15 facilitates the trafficking of NK cells into the lung airways. Blocking IL-15 delays NK cell entry to the site of infection and results in a disregulated control of early viral replication. By the same principle, viral control by NK cells can be therapeutically enhanced via intranasal administration of exogenous IL-15 in the early days post influenza infection. In addition to controlling early viral replication, this IL-15-induced mobilization of NK cells to the lung airways has important downstream consequences on adaptive responses. Primarily, depletion of responding NK1.1+ NK cells is associated with reduced immigration of influenza-specific CD8 T cells to the site of infection. Together this work suggests that local deposits of IL-15 in the lung airways regulate the coordinated innate and adaptive immune responses to influenza infection and may represent an important point of immune intervention.
PMID:
22624047
[PubMed - in process]
Free full text
http://www.ncbi.nlm.nih.gov/pubmed/22624047
IL-15 Participates in the Respiratory Innate Immune Response to Influenza Virus Infection.
Verbist KC, Rose DL, Cole CJ, Field MB, Klonowski KD.
Source
Department of Cellular Biology, University of Georgia, Athens, Georgia, United States of America.
Abstract
Following influenza infection, natural killer (NK) cells function as interim effectors by suppressing viral replication until CD8 T cells are activated, proliferate, and are mobilized within the respiratory tract. Thus, NK cells are an important first line of defense against influenza virus. Here, in a murine model of influenza, we show that virally-induced IL-15 facilitates the trafficking of NK cells into the lung airways. Blocking IL-15 delays NK cell entry to the site of infection and results in a disregulated control of early viral replication. By the same principle, viral control by NK cells can be therapeutically enhanced via intranasal administration of exogenous IL-15 in the early days post influenza infection. In addition to controlling early viral replication, this IL-15-induced mobilization of NK cells to the lung airways has important downstream consequences on adaptive responses. Primarily, depletion of responding NK1.1+ NK cells is associated with reduced immigration of influenza-specific CD8 T cells to the site of infection. Together this work suggests that local deposits of IL-15 in the lung airways regulate the coordinated innate and adaptive immune responses to influenza infection and may represent an important point of immune intervention.
PMID:
22624047
[PubMed - in process]
Free full text
http://www.ncbi.nlm.nih.gov/pubmed/22624047