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γδ T cells and Th17 cytokines in hypersensitivity pneumonitis and lung fibrosis

  • Philip L. Simonian

      Affiliations

    • Department of Medicine, University of Colorado Denver, Aurora, CO
    • Corresponding Author InformationReprint requests: Philip L. Simonian, MD, Divisions of Clinical Immunology and Pulmonary Sciences/Critical Care, Department of Medicine, University of Colorado Denver, 12700 East 19th Avenue, Aurora, CO 80045;
  • ,
  • Christina L. Roark

      Affiliations

    • Integrated Department of Immunology, National Jewish Health, Denver, CO
  • ,
  • Willi K. Born

      Affiliations

    • Integrated Department of Immunology, National Jewish Health, Denver, CO
  • ,
  • Rebecca L. O'Brien

      Affiliations

    • Integrated Department of Immunology, National Jewish Health, Denver, CO
  • ,
  • Andrew P. Fontenot

      Affiliations

    • Department of Medicine, University of Colorado Denver, Aurora, CO
    • Integrated Department of Immunology, National Jewish Health, Denver, CO

Received 26 January 2009; received in revised form 24 June 2009; accepted 29 July 2009. published online 24 August 2009.
Uncorrected Proof

Aurora and Denver, Col

Hypersensitivity pneumonitis (HP) is an inflammatory lung disease caused by repeated inhalation of aerosolized antigens. With chronic exposure to an inhaled antigen, patients are at risk of developing irreversible pulmonary fibrosis and increased morbidity and mortality. Although αβ T cells have been shown to be important in the pathogenesis of HP, γδ T cells are also found and may protect against lung damage and fibrosis caused by chronic exposure to an inhaled pathogen. Th1 cytokines have been implicated in the pathogenesis of HP; yet patients with HP still develop pulmonary fibrosis suggesting that other T-cell cytokines may be involved. Th17 cytokines are a novel group of effector molecules expressed by various T lymphocytes, including γδ T cells. Th17-expressing γδ T cells are important for mucosal immunity against invading microbial pathogens and other inhaled antigens. An increased understanding of γδ T cells that express Th17 cytokines in HP may lead to the development of novel therapeutic and clinical strategies that prevent fibrotic lung disease in patients with HP.

Abbreviations: HP, hypersensitivity pneumonitis

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 Supported by the following grants HL62410 and ES011810 (to A.P.F.) and HL89766 (to P.L.S.) from the National Institutes of Health.

PII: S1931-5244(09)00241-2

doi:10.1016/j.trsl.2009.07.011

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