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  • Conference paper
    Pytel KM, 2015,

    Production of therapeutically relevant levels of FVIII after transduction of lungs with F/HN-pseudotyped lentivirus

    , American Society for Gene and Cell Therapy, 18th Annual Meeting
  • Journal article
    Chiu C, Openshaw PJ, 2015,

    Antiviral B cell and T cell immunity in the lungs

    , NATURE IMMUNOLOGY, Vol: 16, Pages: 18-26, ISSN: 1529-2908
  • Journal article
    Goritzka M, Durant LR, Pereira C, Salek-Ardakani S, Openshaw PJM, Johansson Cet al., 2014,

    Alpha/Beta Interferon Receptor Signaling Amplifies Early Proinflammatory Cytokine Production in the Lung during Respiratory Syncytial Virus Infection

    , Journal of Virology, Vol: 88, Pages: 6128-6136, ISSN: 0022-538X

    Type I interferons (IFNs) are produced early upon virus infection and signal through the alpha/beta interferon (IFN-α/β) receptor (IFNAR) to induce genes that encode proteins important for limiting viral replication and directing immune responses. To investigate the extent to which type I IFNs play a role in the local regulation of inflammation in the airways, we examined their importance in early lung responses to infection with respiratory syncytial virus (RSV). IFNAR1-deficient (IFNAR1−/−) mice displayed increased lung viral load and weight loss during RSV infection. As expected, expression of IFN-inducible genes was markedly reduced in the lungs of IFNAR1−/− mice. Surprisingly, we found that the levels of proinflammatory cytokines and chemokines in the lungs of RSV-infected mice were also greatly reduced in the absence of IFNAR signaling. Furthermore, low levels of proinflammatory cytokines were also detected in the lungs of IFNAR1−/− mice challenged with noninfectious innate immune stimuli such as selected Toll-like receptor (TLR) agonists. Finally, recombinant IFN-α was sufficient to potentiate the production of inflammatory mediators in the lungs of wild-type mice challenged with innate immune stimuli. Thus, in addition to its well-known role in antiviral resistance, type I IFN receptor signaling acts as a central driver of early proinflammatory responses in the lung. Inhibiting the effects of type I IFNs may therefore be useful in dampening inflammation in lung diseases characterized by enhanced inflammatory cytokine production.
  • Journal article
    Schnoeller C, Roux X, Sawant D, Raze D, Olszewska W, Locht C, Openshaw PJet al., 2014,

    Attenuated Bordetella pertussis Vaccine Protects against Respiratory Syncytial Virus Disease via an IL-17-Dependent Mechanism

    , AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 189, Pages: 194-202, ISSN: 1073-449X
  • Journal article
    Durant LR, Makris S, Voorburg CM, Loebbermann J, Johansson C, Openshaw PJMet al., 2013,

    Regulatory T Cells Prevent Th2 Immune Responses and Pulmonary Eosinophilia during Respiratory Syncytial Virus Infection in Mice

    , JOURNAL OF VIROLOGY, Vol: 87, Pages: 10946-10954, ISSN: 0022-538X
  • Journal article
    Tregoning JS, Wang BL, McDonald JU, Yamaguchi Y, Harker JA, Goritzka M, Johansson C, Bukreyev A, Collins PL, Openshaw PJet al., 2013,

    Neonatal antibody responses are attenuated by interferon-gamma produced by NK and T cells during RSV infection

    , PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, Vol: 110, Pages: 5576-5581, ISSN: 0027-8424
  • Journal article
    Loebbermann J, Durant L, Thornton H, Johansson C, Openshaw PJet al., 2013,

    Defective immunoregulation in RSV vaccine-augmented viral lung disease restored by selective chemoattraction of regulatory T cells

    , PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, Vol: 110, Pages: 2987-2992, ISSN: 0027-8424
  • Journal article
    Sridhar S, Begom S, Bermingham A, Ziegler T, Roberts KL, Barclay WS, Openshaw P, Lalvani Aet al., 2012,

    Predominance of heterosubtypic IFN-?-only-secreting effector memory T cells in pandemic H1N1 naive adults

    , EUROPEAN JOURNAL OF IMMUNOLOGY, Vol: 42, Pages: 2913-2924, ISSN: 0014-2980
  • Journal article
    Everitt A, Clare S, Pertel T, John S, Wash R, Smith S, Chin C, Feeley E, Simms J, Adams D, Wise H, Kane L, Goulding D, Digard P, Anttila V, Baillie K, Walsh T, Hume D, Palotie A, Xue Y, Colonna V, Tyler-Smith C, Dunning J, Gordon S, Smyth RS, Openshaw P, Dougan G, Brass A, Kellam Pet al., 2012,

    IFITM3 restricts the morbidity and mortality associated with influenza

    , INTERNATIONAL JOURNAL OF INFECTIOUS DISEASES, Vol: 16, Pages: E79-E79, ISSN: 1201-9712
  • Journal article
    Everitt AR, Clare S, Pertel T, John SP, Wash RS, Smith SE, Chin CR, Feeley EM, Sims JS, Adams DJ, Wise HM, Kane L, Goulding D, Digard P, Anttila V, Baillie JK, Walsh TS, Hume DA, Palotie A, Xue Y, Colonna V, Tyler-Smith C, Dunning J, Gordon SB, GenISIS Investigators, MOSAIC Investigators, Smyth RL, Openshaw PJ, Dougan G, Brass AL, Kellam Pet al., 2012,

    IFITM3 restricts the morbidity and mortality associated with influenza.

    , Nature, Vol: 484, Pages: 519-523

    The 2009 H1N1 influenza pandemic showed the speed with which a novel respiratory virus can spread and the ability of a generally mild infection to induce severe morbidity and mortality in a subset of the population. Recent in vitro studies show that the interferon-inducible transmembrane (IFITM) protein family members potently restrict the replication of multiple pathogenic viruses1, 2, 3, 4, 5, 6, 7. Both the magnitude and breadth of the IFITM proteins’ in vitro effects suggest that they are critical for intrinsic resistance to such viruses, including influenza viruses. Using a knockout mouse model8, we now test this hypothesis directly and find that IFITM3 is essential for defending the host against influenza A virus in vivo. Mice lacking Ifitm3 display fulminant viral pneumonia when challenged with a normally low-pathogenicity influenza virus, mirroring the destruction inflicted by the highly pathogenic 1918 ‘Spanish’ influenza9, 10. Similar increased viral replication is seen in vitro, with protection rescued by the re-introduction of Ifitm3. To test the role of IFITM3 in human influenza virus infection, we assessed the IFITM3 alleles of individuals hospitalized with seasonal or pandemic influenza H1N1/09 viruses. We find that a statistically significant number of hospitalized subjects show enrichment for a minor IFITM3 allele (SNP rs12252-C) that alters a splice acceptor site, and functional assays show the minor CC genotype IFITM3 has reduced influenza virus restriction in vitro. Together these data reveal that the action of a single intrinsic immune effector, IFITM3, profoundly alters the course of influenza virus infection in mouse and humans.

This data is extracted from the Web of Science and reproduced under a licence from Thomson Reuters. You may not copy or re-distribute this data in whole or in part without the written consent of the Science business of Thomson Reuters.

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