Effector CD8+ T cells mediate inflammation and airway hyper-responsiveness.
Nat Med
; 10(8): 865-9, 2004 Aug.
Article
en En
| MEDLINE
| ID: mdl-15258576
ABSTRACT
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.
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Banco de datos:
MEDLINE
Asunto principal:
Bronquitis
/
Alérgenos
/
Subgrupos de Linfocitos T
/
Hiperreactividad Bronquial
/
Linfocitos T CD8-positivos
Límite:
Animals
Idioma:
En
Año:
2004
Tipo del documento:
Article