Journal
EXPERIMENTAL DERMATOLOGY
Volume 31, Issue 8, Pages 1165-1176Publisher
WILEY
DOI: 10.1111/exd.14568
Keywords
HERV; I-IFN; keratinocytes; RIG-I; SLE; UV-B
Categories
Funding
- National Natural Science Foundation of China [82030097]
- CAMS Innovation Fund for Medical Sciences (CIFMS) [2019--I2M--5--033]
- Key project for international and regional cooperation in science and technology innovation of Hunan province [2019WK2081]
Ask authors/readers for more resources
This study reveals that UVB irradiation activates human endogenous retroviruses (HERVs), leading to immune response. The study also suggests that UVB-induced overexpression of HERV-dsRNA promotes the production of type I interferon, which contributes to skin inflammatory response and skin lesions in SLE/DLE.
Skin inflammation and photosensitivity are common in lupus erythematosus (LE) patients, and ultraviolet (UV) light is a known trigger of skin and possibly systemic inflammation in systemic lupus erythematosus (SLE) and discoid lupus erythematosus (DLE) patients. Type I interferons (IFN) are upregulated in LE skin after UV exposure; however, the mechanisms to explain UVB-induced inflammation remain unclear. Here, we demonstrated that UVB irradiation-induced activation of human endogenous retroviruses (HERVs) plays a major role in the immune response. UVB-induced HERV-associated dsRNA transcription and subsequent activation of the innate antiviral RIG-I/MDA5/IRF7 pathway led to downstream transcription of interferon-stimulated genes, which promotes UVB-induced apoptosis and proliferation inhibition in keratinocytes through RIG-I and MDA5 pathways. Our findings indicate that UVB irradiation induces HERV-dsRNA overexpression, and the dsRNA-sensing innate immunity pathway promotes type I IFN production, which may be a potential mechanism of skin inflammatory response and skin lesion of SLE/DLE.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available