Nature Medicine10, 865 - 869 (2004)
Published online: 18 July 2004; | doi:10.1038/nm1081
Effector CD8+ T cells mediate inflammation and airway hyper-responsiveness
Nobuaki Miyahara1, 3, Bradley J Swanson2, 3, Katsuyuki Takeda1, Christian Taube1, Satoko Miyahara1, Taku Kodama1, Azzeddine Dakhama1, Vanessa L Ott2
& Erwin W Gelfand1
1
Division of Cell Biology, Department of Pediatrics, National Jewish Medical and Research Center, Denver, Colorado, USA.
2
Department of Immunology, National Jewish Medical and Research Center, Denver, Colorado, USA.
3
These authors contributed equally to this work.
Correspondence should be addressed to Erwin W Gelfand gelfande@njc.org
Allergic asthma is a complex syndrome characterized by airway obstruction, airway inflammation and airway hyper-responsiveness (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 cells1. Previously, two distinct populations of antigen-experienced CD8+ T cells, termed effector (TEFF) and central memory (TCM) cells, have been described2,
3,
4,
5. 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.
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