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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.

Original publication

DOI

10.1016/j.immuni.2014.06.016

Type

Journal article

Journal

Immunity

Publication Date

21/08/2014

Volume

41

Pages

283 - 295

Keywords

Animals, Antigen Presentation, Cell Communication, Cell Differentiation, Cell Proliferation, Cells, Cultured, Coculture Techniques, Dendritic Cells, Histocompatibility Antigens Class II, Immunity, Cellular, Immunity, Innate, Interleukin-13, Interleukin-2, Lymphocyte Activation, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Mice, Knockout, Nippostrongylus, Th2 Cells