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.

METHODS

Human and mouse ILC2s were assessed for surface expression of β and β integrin adhesion molecules by using flow cytometry. The role of β and β integrins in ILC2 trafficking to the lungs was assessed by in vivo blocking of these integrins before airway exposure to Alternaria in mice.

RESULTS

Both human and mouse lung ILC2s express high levels of β and β integrin adhesion receptors. Intranasal administration of Alternaria challenge reduced ILC2 numbers in the bone marrow and concurrently increased blood and lung ILC2 numbers. In vivo blocking of β integrins (CD18) significantly reduced ILC2 numbers in the lungs but did not alter ILC2 proliferation, apoptosis, and function. In contrast, in vivo blocking of β integrins or α integrins did not affect lung ILC2 numbers.

CONCLUSION

ILC2 numbers increase in the mouse lung not only through local proliferation but also through trafficking from the circulation into the lung using β rather than β or α integrins.