Background/Objective: There is a strong association between RSV infections and episodes of asthma, but the underlying mechanisms are still unclear.The aim of this study is to explore whether RSV infection could break immune toleranceinducing to asthma, and to clarify the role of IL-17 in RSV breakingimmune tolerance.Methods: Establishing a mice model of immune tolerance by oral feeding with OVA, and infected with RSV before arousing airway high reactivity.Neutralizing IL-17A before infected with RSV.After the last challengewith OVA the mice were analyzed for AHR,eosinophil infiltration, levels of cytokines, IgE production,percentage of Th2 and Thl7 cell,and lung histology.Results: After RSV infection, the Tol group developed the re-emergence of symptoms of asthma, such as increased airway pressure, elevated serum IgE and total number of inflammatory ceils in BALF compared with non-infected tolerance group.Quantitative PCR showed that in Tol+RSV group, the mRNA expressions of IL-4、 IL-5、 IL-13 and IL-17A were significantly up-regulated, especially IL-17A.Pathological results showed that inflammatory responses of the lung reappeared again.Flow cytometry results showed the proportion of Th2, Thl7 subsets in infected mice and non-infected were 2.45±0.06% and 2.19%±0.05% respectively, significantly higher than control group (P <0.05).These results proved that RSV could break immune tolerance in mice leading to asthma.IL-17A neutralizing antibodies administration to RSV infection mice significantly reduced airway hyperresponsiveness under different concentrations of Mch (3.125mg/ml, 6.25 mg/ml,12.5mg/ml), serum IgE production (P <0.05) and pathological inflammatory responses in the lung.Flow cytometry results showed the proportions of Th2, Thl7 subsets were1.48±0.05% and 0.48%±0.04%, significantly lower than those of the infected control group.However, the injection of control antibody IgG did not improve early pathophysiological changes caused by RSV infection.Conclusion: Early RSV infection could break immune tolerance of oral OVA and re-induced asthma, which might be due to Th17/IL-17Aup-regulation.IL-17 Ab could inhibit the damaging effects of early RSV infection to immune tolerance mice.