IL-13 from intraepithelial lymphocytes regulates tissue homeostasis and protects against carcinogenesis in the skin
File(s)ncomms12080.pdf (809.69 KB) ncomms12080-s1.pdf (2.34 MB)
Published version
Supporting information
Author(s)
Dalessandri, T
Crawford, G
Hayes, M
Castro Seoane, R
Strid, J
Type
Journal Article
Abstract
The skin is under constant renewal and exposure to environmental challenges. How
homeostasis is maintained alongside protective mechanisms against damage is unclear.
Among the basal epithelial cells (ECs) is a population of resident intraepithelial lymphocytes
(IELs) that provide host-protective immune surveillance. Here we show that IELs
cross-communicate with ECs via the production of IL-13. Skin ECs are activated by IEL-derived
IL-13, enabling a canonical EC stress response. In the absence of IL-13, or canonical IEL, the
skin has decreased ability to repair its barrier and increased susceptibility to cutaneous
carcinogenesis. IL-13 controls the rate of EC movement through the epidermis, which might
explain the importance of IL-13 for epidermal integrity and its suppressive effect on skin
carcinogenesis. These findings show that IL-13 acts as a molecular bridge between IELs and
ECs, and reveal a critical host-defensive role for type-2 immunity in regulating EC tissue
homeostasis and carcinogenesis.
homeostasis is maintained alongside protective mechanisms against damage is unclear.
Among the basal epithelial cells (ECs) is a population of resident intraepithelial lymphocytes
(IELs) that provide host-protective immune surveillance. Here we show that IELs
cross-communicate with ECs via the production of IL-13. Skin ECs are activated by IEL-derived
IL-13, enabling a canonical EC stress response. In the absence of IL-13, or canonical IEL, the
skin has decreased ability to repair its barrier and increased susceptibility to cutaneous
carcinogenesis. IL-13 controls the rate of EC movement through the epidermis, which might
explain the importance of IL-13 for epidermal integrity and its suppressive effect on skin
carcinogenesis. These findings show that IL-13 acts as a molecular bridge between IELs and
ECs, and reveal a critical host-defensive role for type-2 immunity in regulating EC tissue
homeostasis and carcinogenesis.
Date Issued
2016-06-30
Date Acceptance
2016-05-26
Citation
Nature Communications, 2016, 7, pp.1-12
ISSN
2041-1723
Publisher
Nature Publishing Group
Start Page
1
End Page
12
Journal / Book Title
Nature Communications
Volume
7
Copyright Statement
This work is licensed under a Creative Commons Attribution 4.0
International License. The images or other third party material in this
article are included in the article’s Creative Commons license, unless indicated otherwise
in the credit line; if the material is not included under the Creative Commons license,
users will need to obtain permission from the license holder to reproduce the material.
To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
International License. The images or other third party material in this
article are included in the article’s Creative Commons license, unless indicated otherwise
in the credit line; if the material is not included under the Creative Commons license,
users will need to obtain permission from the license holder to reproduce the material.
To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
License URL
Sponsor
Wellcome Trust
Identifier
https://www.nature.com/articles/ncomms12080
Grant Number
100999/Z/13/Z
Subjects
Science & Technology
Multidisciplinary Sciences
Science & Technology - Other Topics
DELTA T-CELLS
THYMIC STROMAL LYMPHOPOIETIN
LYMPHOID STRESS-SURVEILLANCE
TERMINAL DIFFERENTIATION
BIOLOGICAL APPROACH
ATOPIC-DERMATITIS
TYPE-2 IMMUNITY
CANCER
GAMMA
INFLAMMATION
Animals
Cytokines
Epithelial Cells
Homeostasis
Interleukin-13
Interleukin-33
Intraepithelial Lymphocytes
Mice, Inbred BALB C
Skin
Skin Neoplasms
Epithelial Cells
Skin
Animals
Mice, Inbred BALB C
Skin Neoplasms
Interleukin-13
Cytokines
Homeostasis
Interleukin-33
Intraepithelial Lymphocytes
Publication Status
Published
Article Number
12080
Date Publish Online
2016-06-30