Most asthma exacerbations are triggered by virus infections, the majority being caused by human rhinoviruses (RV). In mouse models, gammadeltaT cells have been previously demonstrated to influence allergen-driven airways hyper-reactivity (AHR) and can have antiviral activity, implicating them as prime candidates in the pathogenesis of asthma exacerbations. To explore this, we have used human and mouse models of experimental RV-induced asthma exacerbations to examine gammadeltaT-cell responses and determine their role in the immune response and associated airways disease. In humans, airway gammadeltaT-cell numbers were increased in asthmatic vs. healthy control subjects during experimental infection. Airway and blood gammadeltaT-cell numbers were associated with increased airways obstruction and AHR. Airway gammadeltaT-cell number was also positively correlated with bronchoalveolar lavage (BAL) virus load and BAL eosinophils and lymphocytes during RV infection. Consistent with our observations of RV-induced asthma exacerbations in humans, infection of mice with allergic airways inflammation increased lung gammadeltaT-cell number and activation. Inhibiting gammadeltaT-cell responses using anti-gammadeltaTCR (anti-gammadeltaT-cell receptor) antibody treatment in the mouse asthma exacerbation model increased AHR and airway T helper type 2 cell recruitment and eosinophilia, providing evidence that gammadeltaT cells are negative regulators of airways inflammation and disease in RV-induced asthma exacerbations.