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

Research output: Contribution to journalArticlepeer-review

106 Citations (Scopus)


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
Issue number8
Publication statusPublished - Aug 2004
Externally publishedYes

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)


Dive into the research topics of 'Effector CD8+ T cells mediate inflammation and airway hyper-responsiveness'. Together they form a unique fingerprint.

Cite this