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

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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)

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.

Suggested Citation

  • Tim Dalessandri & Greg Crawford & Mark Hayes & Rocio Castro Seoane & Jessica Strid, 2016. "IL-13 from intraepithelial lymphocytes regulates tissue homeostasis and protects against carcinogenesis in the skin," Nature Communications, Nature, vol. 7(1), pages 1-12, November.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms12080
    DOI: 10.1038/ncomms12080
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