Please use this identifier to cite or link to this item: http://hdl.handle.net/2381/40721
Title: CD1a presentation of endogenous antigens by group 2 innate lymphoid cells.
Authors: Hardman, Clare S.
Chen, Yi-Ling
Salimi, Maryam
Jarrett, Rachael
Johnson, David
Järvinen, Valtteri J.
Owens, Raymond J.
Repapi, Emmanouela
Cousins, David J.
Barlow, Jillian L.
McKenzie, Andrew N. J.
Ogg, Graham
First Published: 22-Dec-2017
Publisher: American Association for the Advancement of Science
Citation: Science Immunology, 2017, 2 (18) eaan5918
Abstract: Group 2 innate lymphoid cells (ILC2) are effectors of barrier immunity, with roles in infection, wound healing, and allergy. A proportion of ILC2 express MHCII (major histocompatibility complex II) and are capable of presenting peptide antigens to T cells and amplifying the subsequent adaptive immune response. Recent studies have highlighted the importance of CD1a-reactive T cells in allergy and infection, activated by the presentation of endogenous neolipid antigens and bacterial components. Using a human skin challenge model, we unexpectedly show that human skin-derived ILC2 can express CD1a and are capable of presenting endogenous antigens to T cells. CD1a expression is up-regulated by TSLP (thymic stromal lymphopoietin) at levels observed in the skin of patients with atopic dermatitis, and the response is dependent on PLA2G4A. Furthermore, this pathway is used to sense Staphylococcus aureus by promoting Toll-like receptor-dependent CD1a-reactive T cell responses to endogenous ligands. These findings define a previously unrecognized role for ILC2 in lipid surveillance and identify shared pathways of CD1a- and PLA2G4A-dependent ILC2 inflammation amenable to therapeutic intervention.
DOI Link: 10.1126/sciimmunol.aan5918
eISSN: 2470-9468
Links: http://immunology.sciencemag.org/content/2/18/eaan5918
http://hdl.handle.net/2381/40721
Version: Post-print
Status: Peer-reviewed
Type: Journal Article
Rights: Copyright © 2017, American Association for the Advancement of Science. Deposited with reference to the publisher’s open access archiving policy.
Appears in Collections:Published Articles, Dept. of Infection, Immunity and Inflammation

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