MHCII-mediated dialog between group 2 innate lymphoid cells and CD4+ T cells potentiates type 2 immunity and promotes parasitic helminth expulsion
Oliphant CJ., Hwang YY., Walker JA., Salimi M., Wong SH., Brewer JM., Englezakis A., Barlow JL., Hams E., Scanlon ST., Ogg GS., Fallon PG., McKenzie ANJ.
Group 2 innate lymphoid cells (ILC2s) release interleukin-13 (IL-13) during protective immunity to helminth infection and detrimentally during allergy and asthma. Using two mouse models to deplete ILC2s invivo, we demonstrate that T helper 2 (Th2) cell responses are impaired in the absence of ILC2s. We show that MHCII-expressing ILC2s interact with antigen-specific Tcells to instigate a dialog in which IL-2 production from Tcells promotes ILC2 proliferation and IL-13 production. Deletion of MHCII renders IL-13-expressing ILC2s incapable of efficiently inducing Nippostrongylus brasiliensis expulsion. Thus, during transition to adaptive Tcell-mediated immunity, the ILC2 and Tcell crosstalk contributes to their mutual maintenance, expansion and cytokine production. This interaction appears to augment dendritic-cell-induced Tcell activation and identifies a previously unappreciated pathway in the regulation of type-2 immunity. © 2014 The Authors.