tetano
Editor, Senior Moderator
J Virol. 2010 May 19. [Epub ahead of print]
Differential activation of NK cells by influenza A pseudotype H5N1 and 1918 and 2009 pandemic H1N1 viruses.
Du N, Zhou J, Lin X, Zhang Y, Yang X, Wang Y, Shu Y.
Key Laboratory for Virus Gene Engineer, National Institute for Viral Disease Control and Prevention, China CDC, 100 Yingxin Street, Xuanwu District, Beijing, 100052, PR China.
Abstract
Natural killer (NK) cells are the effectors of innate immunity and are recruited into the pulmonary 48 h after influenza virus infection. Functional NK cell activation can be triggered by the interaction between viral hemagglutinin (HA) and natural cytotoxicity receptors, NKp46 and NKp44, on cell surface. Recently, novel subtypes of influenza viruses such as H5N1 and 2009 pandemic H1N1 transmitted directly to the human population, with unusual mortality and mobility rates. Here, the human NK cell responses to these viruses were studied. Differential activation of heterogeneous NK cells (upregulation of CD69 and CD107a, and IFN-gamma production as well as downregulation of NKp46) was observed following interactions with H5N1, 1918 H1N1, and 2009 H1N1 pseudotyped particles (pps), respectively, and the responses of CD56(dim) subset predominated. Much stronger NK activation was triggered by H5N1 and 1918 H1N1 pps as compared with 2009 H1N1 pps. The interaction of pps with NK cells and subsequent internalization were mediated by NKp46 partially. The NK cell activation by pps showed a dosage-dependent manner while an increasing viral HA titer attenuated NK activation phenotypes, cytotoxicity, and IFN-gamma production. The various host innate immune responses to different influenza subtypes or HA titers may be associated with disease severity.
PMID: 20484512 [PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/20484512?dopt=Abstract
Differential activation of NK cells by influenza A pseudotype H5N1 and 1918 and 2009 pandemic H1N1 viruses.
Du N, Zhou J, Lin X, Zhang Y, Yang X, Wang Y, Shu Y.
Key Laboratory for Virus Gene Engineer, National Institute for Viral Disease Control and Prevention, China CDC, 100 Yingxin Street, Xuanwu District, Beijing, 100052, PR China.
Abstract
Natural killer (NK) cells are the effectors of innate immunity and are recruited into the pulmonary 48 h after influenza virus infection. Functional NK cell activation can be triggered by the interaction between viral hemagglutinin (HA) and natural cytotoxicity receptors, NKp46 and NKp44, on cell surface. Recently, novel subtypes of influenza viruses such as H5N1 and 2009 pandemic H1N1 transmitted directly to the human population, with unusual mortality and mobility rates. Here, the human NK cell responses to these viruses were studied. Differential activation of heterogeneous NK cells (upregulation of CD69 and CD107a, and IFN-gamma production as well as downregulation of NKp46) was observed following interactions with H5N1, 1918 H1N1, and 2009 H1N1 pseudotyped particles (pps), respectively, and the responses of CD56(dim) subset predominated. Much stronger NK activation was triggered by H5N1 and 1918 H1N1 pps as compared with 2009 H1N1 pps. The interaction of pps with NK cells and subsequent internalization were mediated by NKp46 partially. The NK cell activation by pps showed a dosage-dependent manner while an increasing viral HA titer attenuated NK activation phenotypes, cytotoxicity, and IFN-gamma production. The various host innate immune responses to different influenza subtypes or HA titers may be associated with disease severity.
PMID: 20484512 [PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/20484512?dopt=Abstract