Christopher J. Oliphant 1 , 7 , You Yi Hwang 1 , 7 , Jennifer A. Walker 1 , 7 , Maryam Salimi 2 , See Heng Wong 1 , 8 , James M. Brewer 6 , Alexandros Englezakis 1 , Jillian L. Barlow 1 , Emily Hams 3 , Seth T. Scanlon 1 , Graham S. Ogg 2 , Padraic G. Fallon 3 , 4 , 5 , Andrew N.J. McKenzie 1 , ∗
21 August 2014
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 in vivo, 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 T cells to instigate a dialog in which IL-2 production from T cells 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 T cell-mediated immunity, the ILC2 and T cell crosstalk contributes to their mutual maintenance, expansion and cytokine production. This interaction appears to augment dendritic-cell-induced T cell activation and identifies a previously unappreciated pathway in the regulation of type-2 immunity.
Type-2 innate lymphoid cells proliferate and release interleukin-13 during protective immunity to helminth infection and detrimentally during allergy and asthma. McKenzie and colleagues establish that these activities are potentiated through an MHC class II-mediated dialogue with T cells.