Prevalence of asthma is increasing in westernized countries. Epidemiological studies showed the impact of traffic pollution on the triggering of asthma symptoms and exacerbations, and this effect is mainly attributed to the polycyclic aromatic hydrocarbon core of diesel exhaust particles (DEP). However, although DEP induce IgE synthesis, little is known of their role on T-cell activation, the main cells orchestrating asthma inflammation. We assessed the effect of DEP on T-cell activation in severe uncontrolled asthmatics during (n = 13) and outside (n = 19) exacerbations. Results were compared with data obtained in healthy controls (n = 14). Peripheral blood mononuclear cells were cultured in the presence of low-dose DEP. T-cell activation markers, CD69 and CD25, interleukin-4 (IL-4) and interferon (IFN)-γ production and T-cell proliferation were assessed by flow cytometry. DEP exposure increased the proportion of CD3+CD69+ T cells in all subjects. The proportion of CD25+ T cells increased under DEP stimulation in the exacerbation group only. IFN-γ- and IL-4-producing T cells increased in both asthmatic groups, especially during exacerbations, but not in controls. This effect was more pronounced for IL-4. In response to DEP stimulation, T-cell proliferation increased in higher proportion in asthmatics compared with controls. These results show that DEP activate T cells in asthmatics only, with a higher effect during exacerbations. This is in keeping with epidemiological data which demonstrated that DEP trigger respiratory symptoms in asthmatics but not in controls. The higher effect of DEP in exacerbated asthmatics suggests that uncontrolled asthma is a risk factor for aggravation under exposure to traffic pollutants.