MHCII-Mediated Dialog between Group 2 Innate Lymphoid Cells and CD4(+) T Cells Potentiates Type 2 Immunity and Promotes Parasitic Helminth Expulsion.
Item Type:Journal Article
Citation: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 AN., MHCII-Mediated Dialog between Group 2 Innate Lymphoid Cells and CD4(+) T Cells Potentiates Type 2 Immunity and Promotes Parasitic Helminth Expulsion., Immunity, 41, 2014, 283 - 295
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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.
Science Foundation Ireland (SFI)
Type of material:Journal Article
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