Normality sensing licenses local T cells for innate-like tissue surveillance
© 2022. The Author(s)..
The increasing implication of lymphocytes in general physiology and immune surveillance outside of infection poses the question of how their antigen receptors might be involved. Here, we show that macromolecular aggregates of intraepidermal γδ T cell antigen receptors (TCRs) in the mouse skin aligned with and depended on Skint1, a butyrophilin-like (BTNL) protein expressed by differentiated keratinocytes (KCs) at steady state. Interruption of TCR-mediated 'normality sensing' had no impact on γδ T cell numbers but altered their signature phenotype, while the epidermal barrier function was compromised. In addition to the regulation of steady-state physiology, normality sensing licensed intraepidermal T cells to respond rapidly to subsequent tissue perturbation by using innate tumor necrosis factor (TNF) superfamily receptors. Thus, interfering with Skint1-dependent interactions between local γδ T cells and KCs at steady state increased the susceptibility to ultraviolet B radiation (UVR)-induced DNA damage and inflammation, two cancer-disposing factors.
| Errataetall: |
CommentIn: Nat Immunol. 2022 Mar;23(3):348-349. - PMID 35165447 |
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| Medienart: |
E-Artikel |
| Erscheinungsjahr: |
2022 |
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| Erschienen: |
2022 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:23 |
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| Enthalten in: |
Nature immunology - 23(2022), 3 vom: 11. März, Seite 411-422 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
McKenzie, Duncan R [VerfasserIn] |
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| Links: |
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| Themen: |
Butyrophilins |
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| Anmerkungen: |
Date Completed 14.04.2022 Date Revised 22.10.2022 published: Print-Electronic CommentIn: Nat Immunol. 2022 Mar;23(3):348-349. - PMID 35165447 Citation Status MEDLINE |
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| doi: |
10.1038/s41590-021-01124-8 |
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NLM336975295 |
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| 500 | |a CommentIn: Nat Immunol. 2022 Mar;23(3):348-349. - PMID 35165447 | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a © 2022. The Author(s). | ||
| 520 | |a The increasing implication of lymphocytes in general physiology and immune surveillance outside of infection poses the question of how their antigen receptors might be involved. Here, we show that macromolecular aggregates of intraepidermal γδ T cell antigen receptors (TCRs) in the mouse skin aligned with and depended on Skint1, a butyrophilin-like (BTNL) protein expressed by differentiated keratinocytes (KCs) at steady state. Interruption of TCR-mediated 'normality sensing' had no impact on γδ T cell numbers but altered their signature phenotype, while the epidermal barrier function was compromised. In addition to the regulation of steady-state physiology, normality sensing licensed intraepidermal T cells to respond rapidly to subsequent tissue perturbation by using innate tumor necrosis factor (TNF) superfamily receptors. Thus, interfering with Skint1-dependent interactions between local γδ T cells and KCs at steady state increased the susceptibility to ultraviolet B radiation (UVR)-induced DNA damage and inflammation, two cancer-disposing factors | ||
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| 700 | 1 | |a Bah, Nourdine |e verfasserin |4 aut | |
| 700 | 1 | |a Ushakov, Dmitry S |e verfasserin |4 aut | |
| 700 | 1 | |a Muñoz-Ruiz, Miguel |e verfasserin |4 aut | |
| 700 | 1 | |a Feederle, Regina |e verfasserin |4 aut | |
| 700 | 1 | |a Hayday, Adrian C |e verfasserin |4 aut | |
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