γδ T cells and Th17 cytokines in hypersensitivity pneumonitis and lung fibrosis
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
© 2009 Mosby, Inc. All rights reserved.
