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Updated: Feb 25, 2026
Studying Chronic Exposure of Mice to Ultraviolet B Radiation
Published on: August 19, 2025
IL-1 Receptor-Knockout Mice Develop Epidermal Cysts and Show an Altered Innate Immune Response after Exposure to UVB
Nikhil N Kulkarni1, Christopher A Adase1, Ling-Juan Zhang1
1Department of Dermatology, University of California, San Diego, California, USA.
Abstract:
In this study, we observed that mice lacking the IL-1 receptor (IL-1R) (IL1r-/-) or deficient in IL1-β developed multiple epidermal cysts after chronic UVB exposure. Cysts that developed in IL1r-/- mice were characterized by the presence of the hair follicle marker Sox 9, keratins 10 and 14, and normal melanocyte distribution and retinoid X receptor-α expression. The increased incidence of cysts in IL1r-/- mice was associated with less skin inflammation as characterized by decreased recruitment of macrophages, and their skin also maintained epidermal barrier function compared with wild-type mice. Transcriptional analysis of the skin of IL1r-/- mice after UVB exposure showed decreased gene expression of proinflammatory cytokines such as tumor necrosis factor-α and IL-6. In vitro, primary keratinocytes derived from IL1r-/- mice were more resistant to UVB-triggered cell death compared with wild-type cells, and tumor necrosis factor-α release was completely blocked in the absence of IL-1R. These observations illustrate an unexpected yet prominent phenotype associated with the lack of IL-1R signaling in mice and support further investigation into the role of IL-1 ligands in epidermal repair and innate immune response after damaging UVB exposure.
Insights
Mice lacking the IL-1 receptor (IL-1R) developed epidermal cysts after UVB exposure, showing reduced inflammation and better skin barrier function. This suggests IL-1R signaling impacts skin repair and immunity following UV damage.
Area of Science:
- Dermatology
- Immunology
- Molecular Biology
Background:
- Interleukin-1 (IL-1) signaling plays a role in skin inflammation and immune responses.
- Chronic ultraviolet B (UVB) exposure can lead to skin damage and inflammatory conditions.
Purpose of the Study:
- To investigate the role of IL-1 receptor (IL-1R) signaling in skin responses to chronic UVB exposure.
- To characterize the development of skin lesions in mice deficient in IL-1R or IL-1β after UVB irradiation.
Main Methods:
- Utilized IL-1R knockout (IL1r-/-) and wild-type mice subjected to chronic UVB exposure.
- Analyzed skin histology, including hair follicle markers, melanocyte distribution, and epidermal barrier function.
- Performed transcriptional analysis of skin tissue and in vitro studies on primary keratinocytes.
Main Results:
- IL1r-/- mice developed multiple epidermal cysts post-UVB, distinct from wild-type mice.
- These cysts showed specific markers (Sox9, K10, K14) and normal melanocyte characteristics.
- IL1r-/- mice exhibited reduced skin inflammation, decreased macrophage infiltration, and preserved epidermal barrier function.
- UVB-exposed skin from IL1r-/- mice showed lower expression of pro-inflammatory cytokines (TNF-α, IL-6).
- IL1r-/- keratinocytes were more resistant to UVB-induced cell death and blocked TNF-α release.
Conclusions:
- Absence of IL-1R signaling leads to epidermal cyst formation and altered skin repair after UVB exposure.
- IL-1R signaling contributes to UVB-induced skin inflammation and barrier dysfunction.
- IL-1 ligands are implicated in the skin's innate immune response and repair mechanisms following UV damage.
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