β integrins rather than β integrins mediate Alternaria-induced group 2 innate lymphoid cell trafficking to the lung.

Background: Group 2 innate lymphoid cells (ILC2s) expand in the lungs of mice during type 2 inflammation induced by the fungal allergen Alternaria alternata. The increase in ILC2 numbers in the lung has been largely attributed to local proliferation and whether ILC2s migrate from the circulation to the lung after Alternaria exposure is unknown.

Objective: We examined whether human (lung, lymph node, and blood) and mouse lung ILC2s express β and β integrin adhesion molecules and whether these integrins are required for trafficking of ILC2s into the lungs of mice.