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Immunity. 2014 Aug 21;41(2):283-95. doi: 10.1016/j.immuni.2014.06.016. Epub 2014 Jul 31.

MHCII-mediated dialog between group 2 innate lymphoid cells and CD4(+) T cells potentiates type 2 immunity and promotes parasitic helminth expulsion.

Author information

1
MRC Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge, CB2 0QH, UK.
2
MRC Human Immunology Unit, NIHR Biomedical Research Centre, University of Oxford, John Radcliffe Hospital, OX3 9DS, UK.
3
Institute of Infection, Immunity and Inflammation, GRBC, University Place, Glasgow, G12 8TA, UK.
4
Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin 2, Ireland.
5
Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin 2, Ireland; National Children's Research Centre, Our Lady's Children's Hospital, Crumlin, Dublin 12, Ireland; Institute of Molecular Medicine, Trinity College Dublin, Dublin 2, Ireland.
6
MRC Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge, CB2 0QH, UK. Electronic address: anm@mrc-lmb.cam.ac.uk.

Abstract

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.

PMID:
25088770
PMCID:
PMC4148706
DOI:
10.1016/j.immuni.2014.06.016
[Indexed for MEDLINE]
Free PMC Article

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