Autophagy Suppresses Toll-Like Receptor 3-Mediated Inflammatory Reaction in Human Epidermal Keratinocytes
- Abstract
- Autophagy, one mechanism of programmed cell death, is fundamental to cellular homeostasis. Previous studies have identified autophagy as a novel mechanism by which cytokines control the immune response. However, its precise role in immune-related inflammatory skin diseases such as psoriasis remains unclear. Thus, this study explored the functional role of autophagy in psoriatic inflammation of epidermal keratinocytes. Strong light chain 3 immunoreactivity was observed in epidermal keratinocytes of both human psoriatic lesions and imiquimod-induced mice psoriatic model, and it was readily induced by polycytidylic acid (poly (I:C)), which stimulates Toll-like receptor 3 (TLR3), in human epidermal keratinocytes in vitro. Rapamycin-induced activation of autophagy significantly reduced poly (I:C)-induced inflammatory reaction, whereas, inhibition of autophagy by 3-methyladeine increased that. Our results indicate that the induction of autophagy may attenuate TLR3-mediated immune responses in human epidermal keratinocytes, thus providing novel insights into the mechanisms underlying the development of inflammatory skin diseases including psoriasis.
- All Author(s)
- X. M. Li
; K. E. Jung
; S. H. Yim
; D. K. Hong
; C. D. Kim
; J. Y. Hong
; H. J. Lee
; S. Y. Lee
; J. E. Kim
; C. W. Park
- Issued Date
- 2020
- Type
- Article
- Keyword
- Animals; Autophagy/*physiology; Cells, Cultured; Cytokines/metabolism; Humans; Inflammation/*metabolism; Keratinocytes/*metabolism; Male; Mice; Mice, Inbred BALB C; Psoriasis/*metabolism; Skin/cytology; Toll-Like Receptor 3/*metabolism
- ISSN
- 2314-6133
- Citation Title
- Biomed Research International
- Citation Volume
- 2020
- Citation Start Page
- 4584626
- Citation End Page
- 4584626
- Language(ISO)
- eng
- DOI
- 10.1155/2020/4584626
- URI
- http://schca-ir.schmc.ac.kr/handle/2022.oak/1552
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