Development of allergic diseases is mainly dominated by the type 2 immune response governed by Th2 cells and group 2 innate lymphoid cells (ILC2), both of which produce interleukin (IL)-4, IL-5 and IL-13. Allergen immunotherapy (AIT) is an only causative treatment for allergic diseases by modification of the type 2 immune response. Although regulatory mechanisms of Th2 cells by AIT have been reported to date, those of ILC2 have not been fully elucidated. Although 50-70% of patients with allergies respond favorably to AIT, these therapies are ineffective for the remaining ~30%. The non-responders exhibit persistent ILC2 in peripheral blood despite long-term treatment of AIT. On the other hand, it has been clinically demonstrated that AIT amplified production of "blocking antibody" IgG4 in peripheral blood. In a murine model of asthma, we demonstrated that AIT-increased IgG1 corresponding to human IgG4 significantly suppresses the proliferation of ILC2. It was found that the murine ILC2 did express mRNA of the inhibitory Fc gamma receptor, FcγRIIB, and the expression level correlated with the severity of allergic responses. These data suggested that AIT-increased IgG1 directly suppresses the proliferation of ILC2 via binding FcγRIIB. Therefore, the IgG1-FcγRIIB axis could be a therapeutic target for the non-responders to AIT.