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IL-15 participates in the respiratory innate immune response to influenza virus infection.

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, i... Full description

Journal Title: PloS one 2012, Vol.7(5), p.e37539
Main Author: Verbist, Katherine C
Other Authors: Rose, David L , Cole, Charles J , Field, Mary B , Klonowski, Kimberly D
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: E-ISSN: 1932-6203 ; DOI: 10.1371/journal.pone.0037539
Link: http://search.proquest.com/docview/1016672697/?pq-origsite=primo
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recordid: proquest1016672697
title: IL-15 participates in the respiratory innate immune response to influenza virus infection.
format: Article
creator:
  • Verbist, Katherine C
  • Rose, David L
  • Cole, Charles J
  • Field, Mary B
  • Klonowski, Kimberly D
subjects:
  • Animals–Drug Effects
  • Bronchoalveolar Lavage–Immunology
  • Cell Movement–Immunology
  • Flow Cytometry–Immunology
  • Immunity, Innate–Pharmacology
  • Interleukin-15–Drug Effects
  • Killer Cells, Natural–Immunology
  • Mice–Immunology
  • Mice, Inbred C57bl–Immunology
  • Orthomyxoviridae Infections–Virology
  • Respiratory System–Virology
  • Interleukin-15
ispartof: PloS one, 2012, Vol.7(5), p.e37539
description: 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.
language: eng
source:
identifier: E-ISSN: 1932-6203 ; DOI: 10.1371/journal.pone.0037539
fulltext: fulltext
issn:
  • 19326203
  • 1932-6203
url: Link


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titleIL-15 participates in the respiratory innate immune response to influenza virus infection.
creatorVerbist, Katherine C ; Rose, David L ; Cole, Charles J ; Field, Mary B ; Klonowski, Kimberly D
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identifierE-ISSN: 1932-6203 ; DOI: 10.1371/journal.pone.0037539
subjectAnimals–Drug Effects ; Bronchoalveolar Lavage–Immunology ; Cell Movement–Immunology ; Flow Cytometry–Immunology ; Immunity, Innate–Pharmacology ; Interleukin-15–Drug Effects ; Killer Cells, Natural–Immunology ; Mice–Immunology ; Mice, Inbred C57bl–Immunology ; Orthomyxoviridae Infections–Virology ; Respiratory System–Virology ; Interleukin-15
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descriptionFollowing 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.
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