Transfer of specific cytotoxic T lymphocytes protects mice inoculated with influenza virus

Yap, K. L.; Ada, G. L.; McKenzie, Ian F. C.

doi:10.1038/273238a0

Cited by 496 publications

(264 citation statements)

References 11 publications

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“…41 Our data demonstrated that pre-administration of Ad vector particles (Ad.null) significantly reduced the number of lymphocytes in the lung. However, as Ad.null administration alone was not sufficient to prevent pulmonary hemorrhage (data not shown), or to increase the survival rate of test animals (Figure 4), a decrease in lymphocytes in the lung in response to Ad.null is unlikely to confer significant therapeutic benefit in this lung injury model.…”

Section: Discussionmentioning

confidence: 60%

Adenovirus-mediated transfer of heme oxygenase-1 cDNA attenuates severe lung injury induced by the influenza virus in mice

et al. 2001

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Section: Discussionmentioning

confidence: 60%

Adenovirus-mediated transfer of heme oxygenase-1 cDNA attenuates severe lung injury induced by the influenza virus in mice

et al. 2001

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“…The role of cellular immune responses in protection against influenza is less clear. Although mice lacking functional class I major histocompatibility complex (MHC) glycoproteins and class I MHC-restricted, CD8 + effector T cells are able to clear influenza virus infections [22], CD8 + cyto-toxic T lymphocytes (CTL) can protect against influenza in the absence of antibodies to influenza [23,24], and CTL responses to influenza have been correlated with protection against influenza in humans [25]. Mice and rhesus macaques immunized with HA VRP developed T cell responses as measured by IFN-γ ELISPOT assay, and CD4 + and CD8 + T cells secreting IFN-γ and TNF-α have been identified by cytokine flow cytometry in PBMC from rhesus macaques immunized with HA VRP (E.A.…”

Section: Discussionmentioning

confidence: 99%

Development and preclinical evaluation of an alphavirus replicon vaccine for influenza

Hubby

Talarico

Maughan

et al. 2007

Vaccine

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We used a propagation-defective, single-cycle, alphavirus replicon vector system to produce viruslike replicon particles (VRP) expressing the hemagglutinin (HA) and neuraminidase (NA) proteins from influenza A/Wyoming/03/2003 (H3N2). Efficient production methods were scaled to produce pilot lots of HA VRP and NA VRP and clinical lots of HA VRP. HA VRP-induced high-titered antibody responses in mice, rabbits and rhesus macaques, as measured by ELISA or hemagglutination inhibition (HI) assays, and robust cellular immune responses in mice and rhesus macaques, as measured by IFN-γ ELISPOT. NA VRP also induced cellular immune responses in mice. A toxicology study with HA VRP and NA VRP in rabbits showed no adverse effects in any parameter. These studies support clinical testing of alphavirus replicon vaccines for influenza.

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Section: Ifn-c-inducible Hla-dra and Ciita Expression Are Inhibited Imentioning

confidence: 99%

“…In this respect, several viruses have been shown to inhibit IFN-c up-regulation of MHC class II expression [22,[37][38][39]. Influenza A virus-specific T cell recognition is critical for host recovery from illness [40,41].To investigate whether influenza A virus possesses the ability to evade the IFN-c-induced immunorecognition mechanism, we evaluated the effect of influenza A virus infection on IFN-cinduced Figure 1. IFN-c induction of HLA-DRa and CIITA expression in A549 cells.…”

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confidence: 99%

Influenza A virus abrogates IFN‐γ response in respiratory epithelial cells by disruption of the Jak/Stat pathway

et al. 2008

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The innate immunity to viral infections induces a potent antiviral response mediated by interferons (IFN). Although IFN-c is detected during the acute stages of illness in the upper respiratory tract secretions and in the serum of influenza A virus-infected individuals, control of influenza A virus is not dependent upon IFN-c as evidenced by studies using anti-IFN-c Ab and IFN-c -/-mice. Thus, we hypothesized that IFN-c is not critical in host survival because influenza A virus has mechanisms to evade the antiviral activity of IFN-c. To test this, A549 cells, an epithelial cell line derived from lung adenocarcinoma, were infected with influenza virus strain A/Aichi/2/68 (H3N2) (Aichi) and/or stimulated with IFN-c to detect IFN-c-stimulated MHC class II expression. Influenza A virus infection inhibited IFN-c-induced up-regulation of HLA-DRa mRNA and the IFN-c induction of class II transactivator (CIITA), an obligate mediator of MHC class II expression. Nuclear translocation of Stat1a upon IFN-c stimulation was significantly inhibited in influenza A virus-infected cells and this was associated with a decrease in Tyr701 and Ser727 phosphorylation of Stat1a. Thus, influenza A virus subverts antiviral host defense mediated by IFN-c through effects on the intracellular signaling pathways. IntroductionInfluenza A viruses are negative-strand RNA viruses that have a segmented genome with a coding capacity for 11 polypeptides. The virus genome is composed of eight different RNA segments, which are tightly associated with the viral nucleoprotein and polymerases in ribonucleoprotein complexes [1]. Influenza A viruses, causing acute infections, continuously escape from recognition by virus neutralizing Ab as a result of accumulation of mutations in their surface glycoproteins hemagglutinin and neuraminidase (antigenic drift) or by introduction of new subtypes of these glycoproteins (antigenic shift) [2,3]. Recent outbreaks of highly pathogenic avian influenza A virus infections in poultry and in humans have raised concerns that a new influenza pandemic will occur in the near future [4]. Thus, prediction of the severity of continuously emerging human influenza virus strains remains a high public health priority, but it is limited by our incomplete understanding of the molecular determinants of pathogenicity in this disease. Although factors dictating the severity of virus disease are complex, interaction between inherent viral properties and host cellular response ultimately determines disease outcome. The first site of viral contact with the host and main target of infection and inflammation is the airway mucosal epithelium. Epithelial cells at the airway mucosal surface have a variety of inflammatory and immune defense mechanisms to deal with virus, including Eur. J. Immunol. 2008. 38: 1559-1573 Immunity to infection expression of cytokines with chemoattractant and proinflammatory functions [5], intercellular adhesion molecule-1 (ICAM-1) [6], IFN regulatory factor 1 (IRF-1) [7], nitric oxide synthase 2 (NOS2) [8], and MHC ...

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Transfer of specific cytotoxic T lymphocytes protects mice inoculated with influenza virus

Cited by 496 publications

References 11 publications

Adenovirus-mediated transfer of heme oxygenase-1 cDNA attenuates severe lung injury induced by the influenza virus in mice

Adenovirus-mediated transfer of heme oxygenase-1 cDNA attenuates severe lung injury induced by the influenza virus in mice

Development and preclinical evaluation of an alphavirus replicon vaccine for influenza

Influenza A virus abrogates IFN‐γ response in respiratory epithelial cells by disruption of the Jak/Stat pathway

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