Allergic disease causes a significant health burden, as 80% of the US population is directly or indirectly affected. Chronic allergic diseases develop after repeated allergen exposure, resulting in immune dysregulation and tissue remodeling. A better understanding of how immune dysregulation occurs is needed to fully understand these diseases and to provide more targeted therapies. To study chronic allergic disease, we used Eosinophilic Esophagitis (EoE) as an ideal system, as it shares many features with other chronic allergic diseases. One feature includes a shift in the inflammatory milieu as increased IFNy signatures are present. However, how IFNy influences immune dysregulation, particularly regulatory B (Bregs) and T cells (Tregs) in chronic allergic disease, has not been studied. Herein, we use EoE patient samples and a food-antigen-driven model of EoE to mechanistically interrogate regulatory lymphocytes in vitro and in vivo. We use gain and loss-of-function approaches to determine the contribution of regulatory lymphocytes to disease outcomes. Finally, we test the effects IFNy signaling has on Bregs and Tregs by using genetic mouse models that lack IFNGR1 on these individual populations. We find that while Bregs and Tregs influence different aspects of EoE pathogenesis, both are dysregulated due to IFNy signaling. These findings have important implications for understanding EoE’s etiology and implementing future therapies that target IFNy.