Phosphorylated signal transducer and activator of transcription 3 in the epidermis in adult‐onset Still's disease

T Takeichi, N Watanabe, Y Muro… - The Journal of …, 2017 - Wiley Online Library
T Takeichi, N Watanabe, Y Muro, S Teshigawara, M Sato, N Ban, M Akiyama
The Journal of Dermatology, 2017Wiley Online Library
Adult‐onset Still's disease (AOSD) is characterized by multiple systemic inflammation of
unknown etiology. Although the typical eruption of AOSD is salmon‐pink rheumatoid rash on
the trunk and extremities, persistent pruritic papules and plaques have also been reported.
Correlations between serum cytokines, including interleukin‐6 and‐18, and disease activity
in AOSD have been reported. Activated signal transducer and activator of transcription 3
(STAT 3) is transported into the nucleus, where it functions as a transcription factor that …
Abstract
Adult‐onset Still's disease (AOSD) is characterized by multiple systemic inflammation of unknown etiology. Although the typical eruption of AOSD is salmon‐pink rheumatoid rash on the trunk and extremities, persistent pruritic papules and plaques have also been reported. Correlations between serum cytokines, including interleukin‐6 and ‐18, and disease activity in AOSD have been reported. Activated signal transducer and activator of transcription 3 (STAT3) is transported into the nucleus, where it functions as a transcription factor that regulates genes involved in cell survival and inflammation. To assess whether STAT3 was phosphorylated in skin samples from AOSD patients, we conducted immunohistochemical analysis of affected and unaffected lesions from four AOSD patients in comparison with 10 normal controls. Quantitative analysis was conducted by measuring the ratio of epidermal keratinocytes with phosphorylated STAT3 (p‐STAT3)‐positive nuclei to total epidermal keratinocytes. p‐STAT3 was found to be more strongly expressed in the nuclei in the epidermis of AOSD than in normal controls. Quantification of the data revealed significant differences in staining for p‐STAT3 between AOSD and normal skin. Our findings suggest that phosphorylation of STAT3 may be a potential therapeutic target for AOSD.
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