title: MicroRNA-155 may be involved in the pathogenesis of atopic dermatitis by modulating the differentiation and function of T helper type 17 (Th17) cells.
abstract: Our aims were to identify the differential expression of microRNA (miR)-155, as well as to explore the possible regulatory effects of miR-155 on the differentiation and function of T helper type 17 (Th17) cells in atopic dermatitis (AD). The Th17 cell percentage and expression levels of miR-155, retinoic acid-related orphan receptor (ROR)γt, interleukin (IL)-17 and suppressor of cytokine signalling-1 (SOCS1) in peripheral CD4(+) T cells, plasma and skin specimens were detected and compared in AD patients and healthy subjects. A miR-155 mimic and an inhibitor were transfected separately into AD CD4(+) T cells to confirm the in-vivo data. The Th17 cell percentage, miR-155 expression, RORγt mRNA expression, IL-17 mRNA expression and plasma concentration were increased significantly in AD patients compared with healthy subjects. Conversely, SOCS1 mRNA expression and plasma concentration were decreased significantly. Similar results were detected in cultured CD4(+) T cells transfected with the miR-155 mimic compared with a miR-155 inhibitor or a negative control. Additionally, there was a sequential decrease in miR-155 expression, as well as RORγt and IL-17 mRNA expression, but an increase in SOCS1 mRNA expression, from AD lesional skin and perilesional skin to normal skin. Positive correlations were found between miR-155 expression and AD severity, Th17 cell percentage, RORγt mRNA expression and IL-17 mRNA expression and plasma concentration, while negative correlations were observed between miR-155 expression and SOCS1 mRNA expression and plasma concentration in AD peripheral circulation and skin lesions. In conclusion, miR-155 is over-expressed and may be involved in AD pathogenesis by modulating the differentiation and function of Th17 cells.
authors.affiliation: Departments of *Dermatology, Binzhou, China.
authors.forename: L
authors.initials: L
authors.lastname: Ma
authors.affiliation: Endocrinology and Metabolism, Binzhou Medical University Hospital, Binzhou, China.
authors.forename: H-B
authors.initials: HB
authors.lastname: Xue
authors.affiliation: Departments of *Dermatology, Binzhou, China.
authors.forename: F
authors.initials: F
authors.lastname: Wang
authors.affiliation: Departments of *Dermatology, Binzhou, China.
authors.forename: C-M
authors.initials: CM
authors.lastname: Shu
authors.affiliation: Departments of *Dermatology, Binzhou, China.
authors.forename: J-H
authors.initials: JH
authors.lastname: Zhang
mesh_terms: D000293:Adolescent; D002454:Cell Differentiation; D002648:Child; D003876:Dermatitis, Atopic / Q000235:genetics* / Q000276:immunology / Q000473:pathology; D005260:Female; D006801:Humans; D020381:Interleukin-17 / Q000096:biosynthesis / Q000097:blood / Q000235:genetics; D008297:Male; D035683:MicroRNAs / Q000037:antagonists & inhibitors / Q000096:biosynthesis / Q000235:genetics*; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3 / Q000096:biosynthesis / Q000235:genetics; D012333:RNA, Messenger / Q000096:biosynthesis; D000071222:Suppressor of Cytokine Signaling 1 Protein; D050826:Suppressor of Cytokine Signaling Proteins / Q000096:biosynthesis / Q000097:blood / Q000235:genetics; D058504:Th17 Cells / Q000166:cytology* / Q000276:immunology*
chemical_list: D020381:Interleukin-17; C524942:MIRN155 microRNA, human; D035683:MicroRNAs; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3; D012333:RNA, Messenger; C108944:SOCS1 protein, human; D000071222:Suppressor of Cytokine Signaling 1 Protein; D050826:Suppressor of Cytokine Signaling Proteins
keywords: IL-7; Th17 cells; atopic dermatitis; miR-155; suppressor of cytokine signalling-1