Lines of mice genetically selected for high (H) or low (L) antibody response and for maximal (AIR MAX) or minimal (AIR MIN) acute inflammatory reaction, in which the opposite extreme potentialities have been clearly defined, offer an appropriate model for investigating the environmental and genetic factors acting on innate and adaptative immunobiological functions. This model has been successfully employed to study the resistance or susceptibility against pathogens and/or toxins. It had been demonstrated that the skin contact with Lonomia obliqua caterpillar bristles induces local inflammation and may elicit severe hemorrhagic disorders. In the present study, blood coagulation time, and the acute inflammatory reaction were scored 24 h after injection of the Lonomia bristles crude extract in a subcutaneous dorsal air pouch. The acute inflammation was determined by the leukocyte concentration in the local exudates. The highest interline differences were observed between the AIR MAX (10 6 cells/ml) and AIR MIN (2×10 5 cells/ml) and this distinct expression involves the number of monocytes, eosinophils and mainly neutrophils. Regarding coagulation, the highest interline difference was observed between the H III and L III mice, and the F 1 [L III×H III] hybrids showed the overdominance of the fast clotting character. The adaptative immune response was evaluated by comparing the anti- Lonomia bristle extract IgG titer among the lines: the antibody titers were higher in the H lines than in the L ones and equivalent in the AIR MAX and AIR MIN mice, in accordance to the phenotype profiles generated by the distinct selective processes. The genetically selected mice lines—AIR MAX, AIR MIN, H I, H III, H G, L III and L G—showed an almost continuous distributions for inflammation, coagulation time and IgG antibody titers, being the interline variances always higher than the intraline ones for the individually measured phenotypes. Altogether, these results suggest the independent polygenic regulation of these traits, being indicative of the genetic control to Lonomia toxin innate and adaptative sensitivity in humans.