The ovalbumin (OVA)-induced airway inflammation in rats is a commonly used model to explore the pathobiology of asthma. However, its susceptibility varies greatly between rat strains, and presently BN rats are preferentially used. Since recruitment of T cells to the lungs depends on the CD26 (dipeptidyl-peptidase IV, DPPIV) expression, F344 rats are a highly relevant rat strain, in particular because CD26 deficient substrains are available. To establish a F344 rat model of asthma we challenged F344 rats using different doses of aerosolized antigen (0%, 1%, 2.5%, 5%, and 7.5% OVA) and compared these effects with intratracheal instillation of OVA (1.5mg/0.3ml). Asthmoid responsiveness was determined by analysis of early airway responsiveness (EAR), antigen specific IgE levels, as well as airway inflammation including the composition of T cell subpopulations in the BAL and lung tissue with special respect to the T cell activation markers CD25 and CD26. Even low allergen doses caused allergen specific EAR and increases of antigen specific IgE levels. However, EAR and IgE levels did not increase dose dependently. Higher concentrations of OVA lead to a dose-dependent increase of several immunological markers of allergic asthma including an influx of eosinophils, T cells, and dendritic cells. Interestingly, a dose dependent increase of CD4⁺CD25⁺CD26⁺ T cells was found in the lungs. Summarizing, we established a novel F344 rat model of aerosolized OVA-induced asthma. Thereby, we found a dose dependent recruitment of cellular markers of allergic asthma including the activated CD4⁺CD25⁺CD26⁺ T cell subpopulation, which has not been described in asthma yet.