<i>Background:</i> Signaling through CD28 family co-receptors regulates activation of CD4⁺ T cells positively and negatively. It has been shown that stimulatory co-receptors such as CD28 and ICOS play critical roles in the induction of allergic airway inflammation. However, the role of B and T lymphocyte attenuator (BTLA), an inhibitory co-receptor expressed preferentially in Th1 cells, in the regulation of allergic airway inflammation remains to be determined. <i>Methods:</i> We examined antigen-induced eosinophil recruitment and cytokine production in the airways in antigen-sensitized BTLA-deficient (BTLA–/–) mice. We also examined antigen-induced cytokine production and cell proliferation of splenic T cells in antigen-sensitized BTLA–/– mice. <i>Results:</i> Antigen-induced eosinophil recruitment and IL-5 production in the airways was enhanced in antigen-sensitized BTLA–/– mice. On the other hand, antigen-induced Th1 and Th2 cytokine production as well as T cell proliferation of splenocytes was normal in BTLA–/–mice. <i>Conclusion:</i> BTLA inhibits antigen-induced eosinophil recruitment into the airways by preventing IL-5 production from Th2 cells.