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Vitamin D modulates the allergic phenotype of dendritic cells in children with atopic dermatitis
Author(s) -
Cristi Francisca,
PerezMateluna Guillermo,
VeraKellet Cristián,
SilvaValenzuela Sergio,
Iturriaga Carolina,
HoyosBachiloglu Rodrigo,
NavarreteDechent Cristián,
Cifuentes Lorena,
Camargo Carlos A.,
Kalergis Alexis M.,
Borzutzky Arturo
Publication year - 2019
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/exd.13873
Subject(s) - atopic dermatitis , immunoglobulin e , immunology , scorad , medicine , phenotype , vitamin d and neurology , allergy , biology , antibody , biochemistry , dermatology life quality index , gene , psoriasis
Vitamin D ( VD ) deficiency has been associated with increased incidence and severity of atopic dermatitis ( AD ), but the mechanisms through which VD may ameliorate AD are unclear. We compared the phenotypic characteristics of circulating myeloid and plasmacytoid dendritic cells ( mDC s and pDC s, respectively) of children with AD vs healthy controls ( HC ) and evaluated if VD can modulate the allergic phenotype of circulating DC s in AD patients. Although there was no difference in frequency of circulating DC s between groups, among children with AD there was an inverse correlation between SCORAD and circulating total DC s and mDC s. In AD , serum IgE concentration correlated with Fcε RI and surface‐bound IgE expression on mDC s and pDC s; pDC s expressing Fcε RI and IgE were significantly increased compared to HC . Ex vivo, 1,25( OH ) 2 D 3 significantly decreased Fcε RI expression on mDC s and surface‐bound IgE on mDC s and pDC s. Oral VD supplementation reduced expression of surface‐bound IgE on pDC s in children with AD . In summary, VD decreases the allergic phenotype of circulating DC s in children with AD , a potential mechanism for how VD supplementation may improve AD severity. Future studies are needed to further assess the role of VD supplementation as an immunomodulatory therapy for AD.