Epidermal Notch1 recruits RORγ+ group 3 innate lymphoid cells to orchestrate normal skin repair

Research output: Contribution to journalArticlepeer-review

Standard

Epidermal Notch1 recruits RORγ+ group 3 innate lymphoid cells to orchestrate normal skin repair. / Li, Zhi; Buckley, Christopher; Hodgkinson, Tom; Gothard, Elizabeth J; Boroumand, Soulmaz; Lamb, Rebecca; Cummins, Ian; Narang, Priyanka; Sawtell, Amy; Coles, Jenny; Leonov, German; Reboldi, Andrea; Cupedo, Tom; Siebel, Christian; Bayat, Ardeshir; Coles, Mark C; Ambler, Carrie A.

In: Nature Communications, Vol. 7, 11394, 21.04.2016.

Research output: Contribution to journalArticlepeer-review

Harvard

Li, Z, Buckley, C, Hodgkinson, T, Gothard, EJ, Boroumand, S, Lamb, R, Cummins, I, Narang, P, Sawtell, A, Coles, J, Leonov, G, Reboldi, A, Cupedo, T, Siebel, C, Bayat, A, Coles, MC & Ambler, CA 2016, 'Epidermal Notch1 recruits RORγ+ group 3 innate lymphoid cells to orchestrate normal skin repair', Nature Communications, vol. 7, 11394. https://doi.org/10.1038/ncomms11394

APA

Li, Z., Buckley, C., Hodgkinson, T., Gothard, E. J., Boroumand, S., Lamb, R., Cummins, I., Narang, P., Sawtell, A., Coles, J., Leonov, G., Reboldi, A., Cupedo, T., Siebel, C., Bayat, A., Coles, M. C., & Ambler, C. A. (2016). Epidermal Notch1 recruits RORγ+ group 3 innate lymphoid cells to orchestrate normal skin repair. Nature Communications, 7, [11394]. https://doi.org/10.1038/ncomms11394

Vancouver

Author

Li, Zhi ; Buckley, Christopher ; Hodgkinson, Tom ; Gothard, Elizabeth J ; Boroumand, Soulmaz ; Lamb, Rebecca ; Cummins, Ian ; Narang, Priyanka ; Sawtell, Amy ; Coles, Jenny ; Leonov, German ; Reboldi, Andrea ; Cupedo, Tom ; Siebel, Christian ; Bayat, Ardeshir ; Coles, Mark C ; Ambler, Carrie A. / Epidermal Notch1 recruits RORγ+ group 3 innate lymphoid cells to orchestrate normal skin repair. In: Nature Communications. 2016 ; Vol. 7.

Bibtex

@article{d8705a3aa16d4205aaa05c534282f66d,
title = "Epidermal Notch1 recruits RORγ+ group 3 innate lymphoid cells to orchestrate normal skin repair",
abstract = "Notch has a well-defined role in controlling cell fate decisions in the embryo and the adult epidermis and immune systems, yet emerging evidence suggests Notch also directs non-cell-autonomous signalling in adult tissues. Here, we show that Notch1 works as a damage response signal. Epidermal Notch induces recruitment of immune cell subsets including RORγ+ ILC3s into wounded dermis; RORγ+ ILC3s are potent sources of IL17F in wounds and control immunological and epidermal cell responses. Mice deficient for RORγ+ ILC3s heal wounds poorly resulting from delayed epidermal proliferation and macrophage recruitment in a CCL3-dependent process. Notch1 upregulates TNFα and the ILC3 recruitment chemokines CCL20 and CXCL13. TNFα, as a Notch1 effector, directs ILC3 localization and rates of wound healing. Altogether these findings suggest that Notch is a key stress/injury signal in skin epithelium driving innate immune cell recruitment and normal skin tissue repair.",
author = "Zhi Li and Christopher Buckley and Tom Hodgkinson and Gothard, {Elizabeth J} and Soulmaz Boroumand and Rebecca Lamb and Ian Cummins and Priyanka Narang and Amy Sawtell and Jenny Coles and German Leonov and Andrea Reboldi and Tom Cupedo and Christian Siebel and Ardeshir Bayat and Coles, {Mark C} and Ambler, {Carrie A}",
year = "2016",
month = apr,
day = "21",
doi = "10.1038/ncomms11394",
language = "English",
volume = "7",
journal = "Nature Communications",
issn = "2041-1723",
publisher = "Springer",

}

RIS

TY - JOUR

T1 - Epidermal Notch1 recruits RORγ+ group 3 innate lymphoid cells to orchestrate normal skin repair

AU - Li, Zhi

AU - Buckley, Christopher

AU - Hodgkinson, Tom

AU - Gothard, Elizabeth J

AU - Boroumand, Soulmaz

AU - Lamb, Rebecca

AU - Cummins, Ian

AU - Narang, Priyanka

AU - Sawtell, Amy

AU - Coles, Jenny

AU - Leonov, German

AU - Reboldi, Andrea

AU - Cupedo, Tom

AU - Siebel, Christian

AU - Bayat, Ardeshir

AU - Coles, Mark C

AU - Ambler, Carrie A

PY - 2016/4/21

Y1 - 2016/4/21

N2 - Notch has a well-defined role in controlling cell fate decisions in the embryo and the adult epidermis and immune systems, yet emerging evidence suggests Notch also directs non-cell-autonomous signalling in adult tissues. Here, we show that Notch1 works as a damage response signal. Epidermal Notch induces recruitment of immune cell subsets including RORγ+ ILC3s into wounded dermis; RORγ+ ILC3s are potent sources of IL17F in wounds and control immunological and epidermal cell responses. Mice deficient for RORγ+ ILC3s heal wounds poorly resulting from delayed epidermal proliferation and macrophage recruitment in a CCL3-dependent process. Notch1 upregulates TNFα and the ILC3 recruitment chemokines CCL20 and CXCL13. TNFα, as a Notch1 effector, directs ILC3 localization and rates of wound healing. Altogether these findings suggest that Notch is a key stress/injury signal in skin epithelium driving innate immune cell recruitment and normal skin tissue repair.

AB - Notch has a well-defined role in controlling cell fate decisions in the embryo and the adult epidermis and immune systems, yet emerging evidence suggests Notch also directs non-cell-autonomous signalling in adult tissues. Here, we show that Notch1 works as a damage response signal. Epidermal Notch induces recruitment of immune cell subsets including RORγ+ ILC3s into wounded dermis; RORγ+ ILC3s are potent sources of IL17F in wounds and control immunological and epidermal cell responses. Mice deficient for RORγ+ ILC3s heal wounds poorly resulting from delayed epidermal proliferation and macrophage recruitment in a CCL3-dependent process. Notch1 upregulates TNFα and the ILC3 recruitment chemokines CCL20 and CXCL13. TNFα, as a Notch1 effector, directs ILC3 localization and rates of wound healing. Altogether these findings suggest that Notch is a key stress/injury signal in skin epithelium driving innate immune cell recruitment and normal skin tissue repair.

U2 - 10.1038/ncomms11394

DO - 10.1038/ncomms11394

M3 - Article

VL - 7

JO - Nature Communications

JF - Nature Communications

SN - 2041-1723

M1 - 11394

ER -