CD48 affects type-2 innate lymphoid cell function and airway hyperreactivity.

The importance of type-2 innate lymphoid cell (ILC2), as well as its function in allergic airway inflammatory diseases, have attracted growing attention over recent years. It is anticipated that further elucidation of ILC2 function and regulatory mechanisms will provide a new perspective on potential therapeutic avenues. Here, we describe CD48 as an ILC2 function regulator. The deletion of CD48 has been demonstrated to impair ILC2 activation and proliferation. Moreover, the deletion of CD48 resulted in a reduction in allergen-induced airway hyperresponsiveness in mice. The diminished function of ILC2s resulting from CD48 deletion was offset by the administration of a PKC be-ta stimulator. Taken together, these results suggest that CD48 signaling activates ILC2s via the PKC be-ta pathway and that CD48 inhibition would be a potential new option for asthma therapy. Overall design: mRNA profiles of mouse lung ILC2s from WT and CD48 KO mice were generated by deep sequencing, in duplicates, using a NextSeq 500.