Journal article
CD1a presentation of endogenous antigens by group 2 innate lymphoid cells
- Abstract:
- Group 2 innate lymphoid cells (ILC2) are potent effectors of barrier immunity, with critical roles in infection, wound healing and allergy. In addition to rapid production of cytokines, a proportion of ILC2 express MHC-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 cell wall components. Here 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 on ILC2 is upregulated by TSLP 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 TLR-dependent CD1a-reactive T cell responses to endogenous ligands. These findings define a new role for ILC2 in lipid surveillance, and identify shared pathways of CD1a- and PLA2G4A-dependent ILC2 inflammation amenable to therapeutic intervention.
- Publication status:
- Published
- Peer review status:
- Peer reviewed
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- Files:
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(Preview, Accepted manuscript, pdf, 406.7KB, Terms of use)
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- Publisher copy:
- 10.1126/sciimmunol.aan5918
Authors
- Publisher:
- American Association for the Advancement of Science
- Journal:
- Science Immunology More from this journal
- Volume:
- 2
- Issue:
- 18
- Pages:
- eaan5918
- Publication date:
- 2017-12-22
- Acceptance date:
- 2017-11-07
- DOI:
- EISSN:
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2470-9468
- Pubs id:
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pubs:812356
- UUID:
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uuid:1d6d51c0-c222-4ffb-80cf-62e5d69e39a1
- Local pid:
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pubs:812356
- Source identifiers:
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812356
- Deposit date:
-
2017-12-22
- ARK identifier:
Terms of use
- Copyright holder:
- Ogg et al
- Copyright date:
- 2017
- Notes:
- Copyright © 2017 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. This is the accepted manuscript version of the article. The final version is available online from American Association for the Advancement of Science at: https://doi.org/10.1126/sciimmunol.aan5918
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