1. Effector CD8+ T cells mediate inflammation and airway hyper-responsiveness
- Author
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Bradley J. Swanson, Katsuyuki Takeda, Erwin W. Gelfand, Vanessa L. Ott, Taku Kodama, Christian Taube, Nobuaki Miyahara, Azzeddine Dakhama, and Satoko Miyahara
- Subjects
Adoptive cell transfer ,Ovalbumin ,CD8 Antigens ,medicine.medical_treatment ,Enzyme-Linked Immunosorbent Assay ,Inflammation ,CD8-Positive T-Lymphocytes ,Biology ,General Biochemistry, Genetics and Molecular Biology ,Mice ,T-Lymphocyte Subsets ,medicine ,Animals ,Cytotoxic T cell ,Bronchitis ,Lung ,Cells, Cultured ,Methacholine Chloride ,Analysis of Variance ,Interleukin-13 ,medicine.diagnostic_test ,Interleukin ,General Medicine ,Allergens ,respiratory system ,Airway obstruction ,Flow Cytometry ,medicine.disease ,Adoptive Transfer ,Mice, Mutant Strains ,respiratory tract diseases ,Disease Models, Animal ,Cytokine ,Bronchoalveolar lavage ,Immunology ,Alum Compounds ,Cytokines ,Bronchial Hyperreactivity ,medicine.symptom ,Bronchoalveolar Lavage Fluid ,CD8 - 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.
- Published
- 2004
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