TY - JOUR
T1 - Airway hyperresponsiveness through synergy of γδ T cells and NKT cells
AU - Jin, Niyun
AU - Miyahara, Nobuaki
AU - Roark, Christina L.
AU - French, Jena D.
AU - Aydintug, M. Kemal
AU - Matsuda, Jennifer L.
AU - Gapin, Laurent
AU - O'Brien, Rebecca L.
AU - Gelfand, Erwin W.
AU - Born, Willi K.
PY - 2007/9/1
Y1 - 2007/9/1
N2 - Mice sensitized and challenged with OVA were used to investigate the role of innate T cells in the development of allergic airway hyperresponsiveness (AHR). AHR, but not eosinophilic airway inflammation, was induced in T cell-deficient mice by small numbers of cotransferred γδ T cells and invariant NKT cells, whereas either cell type alone was not effective. Only Vγ1+Vδ5+ γδ T cells enhanced AHR. Surprisingly, OVA-specific αβ T cells were not required, revealing a pathway of AHR development mediated entirely by innate T cells. The data suggest that lymphocytic synergism, which is key to the Ag-specific adaptive immune response, is also intrinsic to T cell-dependent innate responses.
AB - Mice sensitized and challenged with OVA were used to investigate the role of innate T cells in the development of allergic airway hyperresponsiveness (AHR). AHR, but not eosinophilic airway inflammation, was induced in T cell-deficient mice by small numbers of cotransferred γδ T cells and invariant NKT cells, whereas either cell type alone was not effective. Only Vγ1+Vδ5+ γδ T cells enhanced AHR. Surprisingly, OVA-specific αβ T cells were not required, revealing a pathway of AHR development mediated entirely by innate T cells. The data suggest that lymphocytic synergism, which is key to the Ag-specific adaptive immune response, is also intrinsic to T cell-dependent innate responses.
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U2 - 10.4049/jimmunol.179.5.2961
DO - 10.4049/jimmunol.179.5.2961
M3 - Article
C2 - 17709511
AN - SCOPUS:38449105059
SN - 0022-1767
VL - 179
SP - 2961
EP - 2968
JO - Journal of Immunology
JF - Journal of Immunology
IS - 5
ER -