Kurzfassung

Mice lacking Nuclear Factor of Activated T cells-2 (NFATc2) develop an increase in airway hyperresponsiveness (AHR), airway remodeling and serum IgE levels upon OVA sensitization in the absence of allergen challenge. This phenotype was associated with the presence in the airways of effector CD8+CD122- T cells deficient in IFN-gamma production. The origin of this phenotype in NFATc2 (-/-) mice maps to an expanded population of lung CD8+CD122+ (IL-2R chain) CD127hi (IL-7R chain) long-lived...Mice lacking Nuclear Factor of Activated T cells-2 (NFATc2) develop an increase in airway hyperresponsiveness (AHR), airway remodeling and serum IgE levels upon OVA sensitization in the absence of allergen challenge. This phenotype was associated with the presence in the airways of effector CD8+CD122- T cells deficient in IFN-gamma production. The origin of this phenotype in NFATc2 (-/-) mice maps to an expanded population of lung CD8+CD122+ (IL-2R chain) CD127hi (IL-7R chain) long-lived memory cells. Adoptive transfer of ovalbumin (OVA) specific CD8+ NFATc2 (-/-) T cells enhanced the AHR generated by NFATc2 (-/-) CD4+ T cells in immunodeficient mice and was accompanied by increased IL-17 and reduced IFN-gamma production in the reconstituted mice. Depletion of the memory CD8+CD122+IL-7Rhigh T cell population corrected the defect in IFN-gamma production by effector lung NFATc2 (-/-) CD8+CD122- cells and abrogated the increased AHR observed in NFATc2 (-/-) CD8+ T cell-reconstituted SCID mice. » weiterlesen» einklappen