IL-13 from intraepithelial lymphocytes regulates tissue homeostasis and protects against carcinogenesis in the skin

Tim Dalessandri, Greg Crawford, Mark Hayes, Rocio Castro Seoane and Jessica Strid ()
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Tim Dalessandri: Imperial College London
Greg Crawford: Imperial College London
Mark Hayes: Imperial College London
Rocio Castro Seoane: Imperial College London
Jessica Strid: Imperial College London

Nature Communications, 2016, vol. 7, issue 1, 1-12

Abstract: 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.

Date: 2016
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms12080

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DOI: 10.1038/ncomms12080

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