Abstract
SummaryGroup 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.
Highlights
Group 2 immunity is believed to have evolved to combat parasitic helminth infection, and contributes to wound healing
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
Summary
Group 2 immunity is believed to have evolved to combat parasitic helminth infection, and contributes to wound healing. These responses are characterized by adaptive T helper 2 (Th2) cells expressing interleukin-4 (IL-4), IL-5, and IL-13, B cells secreting immunoglobulin E (IgE), eosinophils, and mast cells. IL-25 and IL-33 have been reported to induce T cell expression of type-2 cytokines, and it is these two epithelium-derived factors that potently induce ILC2s at the initiation of type-2 immunity (Moro et al, 2010; Neill et al, 2010). ILC2-produced IL-13 has been linked to the migration of dendritic cells (DCs) and the support of Th2 cell differentiation (Halim et al, 2014)
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