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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2011-5-4
pubmed:abstractText
Influenza A virus (IAV) infection results in a highly contagious respiratory illness leading to substantial morbidity and occasionally death. In this report, we assessed the in vivo physiological contribution of invariant NKT (iNKT) lymphocytes, a subset of lipid-reactive ?? T lymphocytes, on the host response and viral pathogenesis using a virulent, mouse-adapted, IAV H3N2 strain. Upon infection with a lethal dose of IAV, iNKT cells become activated in the lungs and bronchoalveolar space to become rapidly anergic to further restimulation. Relative to wild-type animals, C57BL/6 mice deficient in iNKT cells (J?18(-/-) mice) developed a more severe bronchopneumonia and had an accelerated fatal outcome, a phenomenon reversed by the adoptive transfer of NKT cells prior to infection. The enhanced pathology in J?18(-/-) animals was not associated with either reduced or delayed viral clearance in the lungs or with a defective local NK cell response. In marked contrast, J?18(-/-) mice displayed a dramatically reduced IAV-specific CD8(+) T cell response in the lungs and in lung-draining mediastinal lymph nodes. We further show that this defective CD8(+) T cell response correlates with an altered accumulation and maturation of pulmonary CD103(+), but not CD11b(high), dendritic cells in the mediastinal lymph nodes. Taken together, these findings point to a role for iNKT cells in the control of pneumonia as well as in the development of the CD8(+) T cell response during the early stage of acute IAV H3N2 infection.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1550-6606
pubmed:author
pubmed:issnType
Electronic
pubmed:day
15
pubmed:volume
186
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5590-602
pubmed:dateRevised
2011-9-14
pubmed:meshHeading
pubmed-meshheading:21490153-Adoptive Transfer, pubmed-meshheading:21490153-Animals, pubmed-meshheading:21490153-Antigens, CD, pubmed-meshheading:21490153-Antigens, CD11b, pubmed-meshheading:21490153-Bronchopneumonia, pubmed-meshheading:21490153-CD8-Positive T-Lymphocytes, pubmed-meshheading:21490153-Dendritic Cells, pubmed-meshheading:21490153-Enzyme-Linked Immunosorbent Assay, pubmed-meshheading:21490153-Inflammation, pubmed-meshheading:21490153-Influenza A Virus, H3N2 Subtype, pubmed-meshheading:21490153-Integrin alpha Chains, pubmed-meshheading:21490153-Lung, pubmed-meshheading:21490153-Lymphocyte Activation, pubmed-meshheading:21490153-Mice, pubmed-meshheading:21490153-Mice, Inbred C57BL, pubmed-meshheading:21490153-Natural Killer T-Cells, pubmed-meshheading:21490153-Orthomyxoviridae Infections, pubmed-meshheading:21490153-Pneumonia, Viral, pubmed-meshheading:21490153-Polymerase Chain Reaction, pubmed-meshheading:21490153-Viral Load
pubmed:year
2011
pubmed:articleTitle
Potential role of invariant NKT cells in the control of pulmonary inflammation and CD8+ T cell response during acute influenza A virus H3N2 pneumonia.
pubmed:affiliation
Institut Pasteur de Lille, Centre d'Infection et d'Immunité de Lille, F-59019 Lille, France.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't