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Phosphorylated signal transducer and activator of transcription 3 in the epidermis in adult‐onset Still's disease
Author(s) -
Takeichi Takuya,
Watanabe Naoki,
Muro Yoshinao,
Teshigawara Shiho,
Sato Motoki,
Ban Nobutaro,
Akiyama Masashi
Publication year - 2017
Publication title -
the journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.9
H-Index - 65
eISSN - 1346-8138
pISSN - 0385-2407
DOI - 10.1111/1346-8138.13888
Subject(s) - stat protein , stat , stat3 , medicine , phosphorylation , transcription factor , activator (genetics) , rash , epidermis (zoology) , immunohistochemistry , inflammation , pathology , interleukin 6 , real time polymerase chain reaction , stat6 , immunology , biology , gene , cytokine , microbiology and biotechnology , interleukin 4 , anatomy , receptor , biochemistry
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 regulates genes involved in cell survival and inflammation. To assess whether STAT 3 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 STAT 3 (p‐ STAT 3)‐positive nuclei to total epidermal keratinocytes. p‐ STAT 3 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‐ STAT 3 between AOSD and normal skin. Our findings suggest that phosphorylation of STAT 3 may be a potential therapeutic target for AOSD .