
Airway responsiveness (AR) is determined by complex mechanisms reflecting lung responses to airborne stimuli. Murine studies have identified a number of potential factors modulating AR and thus have contributed to the current understanding of these mechanisms. In allergic inflammation, immune cells, in particular alphabeta T cells, have emerged as important contributors to increased AR. We have found that in contrast to alphabeta T cells, gammadelta T cells can have a negative regulatory effect on AR. Here, we review the current studies on gammadelta T cells in allergic inflammation and discuss their role in modulating AR. We propose that gammadelta T cells exhibit different immune properties depending on the type of stimulus and inflammation. These differential immune properties appear to be associated with specific gammadelta T cell subsets, which control AR to airborne stimuli. In particular, our recent data indicate that the Vgamma4(+) T cell subset acts as an important negative regulator of AR and contributes to maintaining normal lung function in mice.
Disease Models, Animal, Mice, T-Lymphocyte Subsets, Respiratory Hypersensitivity, Animals, Down-Regulation, Humans
Disease Models, Animal, Mice, T-Lymphocyte Subsets, Respiratory Hypersensitivity, Animals, Down-Regulation, Humans
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