Background Viral pathogen–associated molecular patterns, such as dsRNA, disrupt airway tolerance to inhaled allergens. Specifically, the Th2 and Th17 cell responses are induced by low‐dose dsRNA and the Th1‐dominant response by high‐dose dsRNA. Objective In this model, we evaluate the role of TNF‐α in the development of adaptive immune dysfunction to inhaled allergens induced by airway sensitization with dsRNA‐containing allergens. Methods A virus‐associated asthma mouse model was generated via simultaneous airway administration of ovalbumin (OVA) and low (0.1 μg) or high (10 μg) doses of polyinosine–polycytidylic acid (polyI:C). The effect of TNF‐α on Th2 airway inflammation was evaluated using TNF‐α‐deficient mice and recombinant TNF‐α. Results TNF‐α production was enhanced by airway exposure to low and high doses of polyI:C. After airway sensitization with OVA plus low‐dose polyI:C, TNF‐α‐deficient mice exhibited less OVA‐induced airway inflammation than did wild‐type (WT) mice. However, this did not occur upon sensitization with high‐dose polyI:C. In terms of T‐cell response, the production of IL‐4 from lung T cells after OVA challenge was enhanced by airway sensitization with OVA plus low‐dose polyI:C in WT mice, and this phenotype was inhibited by the absence of TNF‐α. Moreover, the Th2 cell response induced by sensitization with OVA plus low‐dose polyI:C, which was abolished in TNF‐α‐deficient mice, was restored in these mice upon addition of recombinant TNF‐α. Conclusion The results of this study suggest that TNF‐α produced by airway exposure to low‐dose dsRNA is a key mediator in the development of Th2 cell response to inhaled allergens.