Group 2 innate lymphoid cells (ILC2s) have been shown to expand in the airways during type 2 inflammation. However whether the increase in ILC2 numbers is due to local proliferation or migration from the circulation remains controversial. In this study, we demonstrate that following challenge with the fungal allergen Alternaria alternata, ILC2s in the lungs of bone marrow transplanted mice are of donor origin and thus demonstrating that ILC2s can migrate to the lungs. In addition, we show that irradiation of IL-7R-/- mice (which lack ILC2s) and subsequent transplantation of wildtype bone marrow results in significant levels of ILC2s in the lungs, compared to naïve IL-7R-/- mice. We investigated the role of integrins in ILC2 migration as leukocytes primarily traffic from the circulation into the tissues utilizing β1 and β2 integrins. Our data suggests that while ILC2s express both β1 and β2 integrins, the major contributors to ILC2 migration to the airways are β2 integrins and more specifically αLβ2. In vivo administration of a β2 integrin blocking antibody significantly diminished ILC2 levels in the lungs following Alternaria challenge. This was likely a direct effect of blocking the interaction between β2 integrins on ILC2s and intercellular adhesion molecule-1 (ICAM-1) in the vasculature, as blocking of β2 integrins on sorted ILC2s diminished adhesion to ICAM-1 in vitro. These findings suggest that during allergic inflammation, ILC2s traffic from the circulation into the tissues using firm adhesions between ILC2 β2 integrins and vascular ICAM-1.