Despite extensive investigation of the signals required for development of T helper type 1 (Th1) and type 2 (Th2) immune responses, the mechanisms involved are still not well‐defined. A critical role for Epstein–Barr virus‐induced gene 3 (EBI3) in these responses has been proposed. EBI3, initially discovered as a transcriptionally activated gene in Epstein–Barr virus‐infected B lymphocytes, codes for a subunit of the cytokine interleukin‐27 (IL‐27). While initial studies suggested that it had an important role in promoting Th1 responses, subsequent studies have revealed that EBI3 receptor signalling influences a variety of immune cell types and can inhibit both Th1 and Th2 responses. In the present study, we evaluated EBI3^−/− mice for their ability to mount both Th1‐mediated and Th2‐mediated airway inflammatory responses. The EBI3^−/− mice sensitized by exposure to inhaled ovalbumin plus a high dose of lipopolysaccharide, which normally results in Th1 responses in wild‐type (WT) mice, instead developed Th2 type airway inflammation, with increased numbers of eosinophils. The EBI3^−/− mice that were exposed to inhaled ovalbumin with a low dose of lipopolysaccharide, which induces Th2 responses in WT mice, showed a marked enhancement of these responses, with increased airway eosinophils, increased serum IgE levels and increased levels of Th2 cytokines (IL‐4, IL‐5 and IL‐13) in culture supernatants of mediastinal lymph node cells. Increased production of Th2 cytokines was also seen when naive CD4⁺ T cells from EBI3^−/− mice were stimulated in vitro compared with cells from WT mice. These results provide the first evidence that EBI3 may play an inhibitory role in allergic asthma development.