Abstract Asthma is a major public health concern affecting millions of people each year. Allergic asthma is a T helper 2 (Th2) cell mediated inflammatory disease characterized by airway inflammation and hyper responsiveness. The Tec family tyrosine kinase Interleukin-2 Inducible T cell kinase (Itk) is primarily expressed in T cells and is critical for development, function and differentiation of T helper cells. Itk-/- mice have a defective Th2 response and are not susceptible to allergic asthma and parasitic worm infections. We observed that naïve CD4+ T cells from Itk-/- mice have substantially increased transcript levels of prototypic Th1 genes. We hypothesized that this upregulation of Th1 genes could negatively regulate polarization to Th2 effector cells. Here, we show that Itk can negatively regulate IFNγ. More importantly, in absence of IFNγ there is a rescue in the expression of Th2 related genes and Th2 mediated allergic asthma in Itk-/- mice. In the absence of Itk, IFNγ levels increase leading to a positive feed-forward loop with T-bet. This is responsible for the inability of CD4+ T cells from Itk-/- mice to optimally induce Th2 transcriptional program and develop a Th2 response upon allergen challenge. In addition to providing mechanistic insight into the observed Th2 defects in Itk-/- mice, this work has implications for understanding Itk as a potential target for Th2 mediated inflammation, T helper differentiation programs and the molecular pathology of asthma.