Effector CD8+ T cells mediate inflammation and airway hyper-responsiveness

Nobuaki Miyahara, Bradley J. Swanson, Katsuyuki Takeda, Christian Taube, Satoko Miyahara, Taku Kodama, Azzeddine Dakhama, Vanessa L. Ott, Erwin W. Gelfand

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152 Citations (Scopus)

Abstract

Allergic asthma is a complex syndrome characterized by airway obstruction, airway inflammation and airway hyperresponsiveness (AHR). Using a mouse model of allergen-induced AHR, we previously demonstrated that CD8-deficient mice develop significantly lower AHR, eosinophilic inflammation and interleukin (IL)-13 levels in bronchoalveolar lavage fluid compared with wild-type mice. These responses were restored by adoptive transfer of antigen-primed CD8 + T cells. Previously, two distinct populations of antigen-experienced CD8+ T cells, termed effector (TEFF) and central memory (TCM) cells, have been described. After adoptive transfer into CD8-deficient mice, TEFF, but not TCM, cells restored AHR, eosinophilic inflammation and IL-13 levels. TEFF, but not TCM, cells accumulated in the lungs, and intracellular cytokine staining showed that the transferred TEFF cells were a source of IL-13. These data suggest an important role for effector CD8+ T cells in the development of AHR and airway inflammation, which may be associated with their Tc2-type cytokine production and their capacity to migrate into the lung.

Original languageEnglish
Pages (from-to)865-869
Number of pages5
JournalNature Medicine
Volume10
Issue number8
DOIs
Publication statusPublished - Aug 1 2004
Externally publishedYes

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

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    Miyahara, N., Swanson, B. J., Takeda, K., Taube, C., Miyahara, S., Kodama, T., Dakhama, A., Ott, V. L., & Gelfand, E. W. (2004). Effector CD8+ T cells mediate inflammation and airway hyper-responsiveness. Nature Medicine, 10(8), 865-869. https://doi.org/10.1038/nm1081