Premium
Biomarkers of alopecia areata disease activity and response to corticosteroid treatment
Author(s) -
FuentesDuculan Judilyn,
Gulati Nicholas,
Bonifacio Kathleen M.,
Kunjravia Norma,
Zheng Xiuzhong,
SuárezFariñas Mayte,
Shemer Avner,
GuttmanYassky Emma,
Krueger James G.
Publication year - 2016
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.12918
Subject(s) - alopecia areata , scalp , medicine , hair follicle , immunology , immune system , ccl17 , cytokine , interleukin , pathology , cxcl10 , chemokine , dermatology
Alopecia areata ( AA ) is a common inflammatory disease targeting the anagen‐stage hair follicle. Different cytokines have been implicated in the disease profile, but their pathogenic role is not yet fully determined. We studied biopsies of pretreatment lesional and non‐lesional ( NL ) scalp and post‐treatment (intra‐lesional steroid injection) lesional scalp of 6 patchy patients with AA using immunohistochemistry and gene expression analysis. Immunohistochemistry showed increases in CD 3 + , CD 8 + T cells, CD 11c + dendritic cells and CD 1a + Langerhans cells within and around hair follicles of pretreatment lesional scalp, which decreased upon treatment. qRT ‐ PCR showed in pretreatment lesional scalp (compared to NL ) significant increases ( P < 0.05) in expression of inflammatory markers ( IL ‐2, IL ‐2 RA , JAK 3, IL ‐15), Th1 ( CXCL 10 and CXCL 9), Th2 ( IL ‐13, CCL 17 and CCL 18), IL ‐12/ IL ‐23p40 and IL ‐32. Among these, we observed significant downregulation with treatment in IL ‐12/ IL ‐23p40, CCL 18 and IL ‐32. We also observed significant downregulation of several hair keratins in lesional scalp, with significant upregulation of KRT 35, KRT 75 and KRT 86 in post‐treatment lesional scalp. This study shows concurrent activation of Th1 and Th2 immune axes as well as IL ‐23 and IL ‐32 cytokine pathways in lesional AA scalp and defined a series of response biomarkers to corticosteroid injection. Clinical trials with selective antagonists coupled with cytokine‐pathway biomarkers will be necessary to further dissect pathogenic immunity.