Oxidative DNA Damage Accelerates Skin Inflammation in Pristane-Induced Lupus Model

September 2020 in “ Frontiers in Immunology ”

Gantsetseg Tumurkhuu, Shuang Chen, Erica N. Montano, Duygu Ercan Laguna, Gabriela De Los Santos, Jeong Min Yu, Malcolm Lane, M Yamashita, Janet L. Markman, Luz P. Blanco, Mariana J. Kaplan, Kenichi Shimada, Timothy R. Crother, Mariko Ishimori, Daniel J. Wallace, Caroline A. Jefferies, Moshe Arditi

oxidative DNA damage oxyguanine glycosylase 1 OGG1 pristane-induced lupus model Systemic Lupus Erythematosus SLE inflammation auto-antibodies skin pathology hair loss thicker epidermis type I interferon IFN cGAS-STING pathway STING inhibitor monocytes lesional skin lupus thicker skin

TLDR Loss of OGG1 increases skin inflammation and auto-antibodies in lupus.

The study concluded that oxidative DNA damage accelerated skin inflammation in a pristane-induced lupus model, with Ogg1-deficient (Ogg1−/−) mice showing increased inflammatory responses, hair loss, and skin pathology compared to wild-type mice. The findings highlighted the role of the DNA repair enzyme OGG1 in mitigating type I interferon responses and inflammation through the cGAS-STING pathway. Reduced OGG1 expression was also observed in SLE patients with skin involvement, suggesting that targeting oxidative DNA damage could be a potential therapeutic strategy for managing SLE-related skin inflammation.

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