Especially, a high level of resemblance at the immunological level has been found, suggesting that mouse models can yield a relevant insight into human pathology. Maximum genetic uniformity can be achieved when using inbred strains. Environmental factors such as exposure to light, diet, air quality and climate can influence the phenotypic outcome of asthma. Using different inbred strains of mice gives the opportunity to estimate the influence of the genetic background on the phenotypical outcome of chemical-induced asthma. Starting from an established mouse model of chemical-induced asthma developed by Vanoirbeek et al. in BALB/c mice, 6 other inbred mouse strains were tested on their sensitizing capacity to toluene-2,4-diisocyanate. By testing different mouse strains we have the opportunity to evaluate the intra- and the inter-strain variability, giving us the possibility to select the inbred mouse strain which represents best the phenotype of human occupational asthma. Seven mouse strains were tested in an established mouse model of chemical-induced asthma. The main findings of this study were that, in general, Th2-biased mice reproduce better than Th1-biased mice, the features that characterize human occupational asthma. BALB/c mice showed the most pronounced differences in AHR, airway inflammation and immunologic parameters, when compared to the two other Th2-biased mouse strains tested. Th1-biased mice, however, were not completely non-responsive. Mice are the most commonly used species to develop experimental models of human diseases. Mice are easy to breed, economical to house and relatively easy to work with. Furthermore, the mouse genome has been extensively studied and it exhibits a high degree of homology with the human genome. Further advantages are the wide variety of available immunological and molecular reagents as well as transgenic animals. Besides the many advantages of animal models, there is still a lot of controversy concerning the use of animals to study human disease. Thus, mice do not spontaneously exhibit symptoms consistent with asthma. Different treatment protocols have been developed to mimic the phenotypes of human asthma, but no mouse model is currently able to mimic the full range of clinical manifestations. Furthermore, important differences exist in airway development and morphology between humans and mice. Mouse airways have fewer airway generations and do not contain smooth muscle bundles. Nevertheless, although mice RAD001 cannot be considered as perfect surrogates for humans, they can be used to test hypotheses in a relatively simple controlled system. In view of the above considerations, it is important to standardize techniques and protocols used, to be able to compare the results of different research groups. So far, the influence of the genetic background of mice on ventilatory and immunological parameters has not been studied much. Our study is one of the first to have compared multiple endpoints of immune-mediated asthma in a large number of inbred mouse strains.