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Oral tolerance modulates the skin transcriptome in mice with induced atopic dermatitis
Author(s) -
Baek J. O.,
Lee J. R.,
Roh J. Y.,
Jung Y.
Publication year - 2018
Publication title -
allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.363
H-Index - 173
eISSN - 1398-9995
pISSN - 0105-4538
DOI - 10.1111/all.13367
Subject(s) - downregulation and upregulation , atopic dermatitis , immunology , inflammation , transcriptome , sensitization , immune system , allergic inflammation , immune tolerance , medicine , gene , gene expression , biology , genetics
Defective gut immune reactions have been implicated in the development of atopic dermatitis ( AD ), whereas oral tolerance ( OT ), that is, the immune unresponsiveness induced by oral antigen administration, protects mice against AD . To investigate this protective role of OT , the transcriptomic profiles of skin were obtained by RNA sequencing from mice that were epicutaneously sensitized, orally tolerized prior to epicutaneous sensitization, or neither (control). Oral tolerance inhibited the upregulation of keratin‐ and allergic inflammation‐associated genes that occurred in the epicutaneously sensitized group. Compared to the controls, mice that were orally tolerized and epicutaneously sensitized showed an upregulation of genes that regulate inflammation or keratinocyte differentiation. Knocking down two of those genes, SCGB 1A1 and TSC 22D3 , upregulated Th2 inflammatory mediators and downregulated a cornified cell envelope‐related gene. Based on our findings, OT may protect skin against allergic inflammation by promoting the expression of genes that regulate Th2 inflammatory responses and skin barrier function.