| First Author | Miyahara N | Year | 2004 |
| Journal | Nat Med | Volume | 10 |
| Issue | 8 | Pages | 865-9 |
| PubMed ID | 15258576 | Mgi Jnum | J:91610 |
| Mgi Id | MGI:3047526 | Doi | 10.1038/nm1081 |
| Citation | Miyahara N, et al. (2004) Effector CD8(+) T cells mediate inflammation and airway hyper-responsiveness. Nat Med 10(8):865-9 |
| abstractText | 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 cells. Previously, two distinct populations of antigen-experienced CD8(+) T cells, termed effector (T(EFF)) and central memory (T(CM)) cells, have been described. After adoptive transfer into CD8-deficient mice, T(EFF), but not T(CM), cells restored AHR, eosinophilic inflammation and IL-13 levels. T(EFF), but not T(CM), cells accumulated in the lungs, and intracellular cytokine staining showed that the transferred T(EFF) 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. |
