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.
Highlights
Psoriasis is a chronic immune-mediated inflammatory skin disease characterized by distinct erythematous plaques with silvery scales, affecting approximately 2 to 3% of the population worldwide [1, 2]
Skin-resident keratinocytes act as inducers of BioMed Research International innate immune responses in the early phase, they are involved in adaptive immune responses and serve as a reservoir of inflammatory mediators necessary for sustained psoriatic lesions [3]
light chain 3 (LC3) was weakly detected in normal epidermis, while strong LC3 immunoreactivity was observed in epidermal keratinocytes in psoriatic lesions (Figure 1(a))
Summary
Psoriasis is a chronic immune-mediated inflammatory skin disease characterized by distinct erythematous plaques with silvery scales, affecting approximately 2 to 3% of the population worldwide [1, 2]. Psoriasis cannot be considered uniquely as a T cell-dependent disease [3], as dysregulated cross talk between immune cells and skin-resident keratinocytes is thought to be essential in psoriasis development [4,5,6]. Skin-resident keratinocytes act as inducers of BioMed Research International innate immune responses in the early phase, they are involved in adaptive immune responses and serve as a reservoir of inflammatory mediators necessary for sustained psoriatic lesions [3]
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