title: Increased plasma LIGHT levels in patients with atopic dermatitis.
abstract: LIGHT [the name of which is derived from 'homologous to lymphotoxins, exhibits inducible expression, competes with herpes simplex virus glycoprotein D for herpes simplex virus entry mediator (HVEM), and expressed by T lymphocytes'], is a member of the tumour necrosis factor superfamily that is involved in various inflammatory diseases. We aimed to estimate the relevance of plasma LIGHT levels as a biomarker for atopic dermatitis (AD). In order to understand the putative role of LIGHT in AD pathogenesis, we also investigate the effects of LIGHT on a monocytic cell line, human acute monocytic leukaemia cell line (THP-1). We examined plasma LIGHT levels, total serum IgE, serum value of CCL17 and peripheral blood eosinophil counts in patients with AD and healthy subjects. The effects of LIGHT on activation and apoptosis in THP-1 cells were also investigated. The plasma concentrations of LIGHT in AD patients were significantly higher than those in healthy individuals and the concentrations decreased as the symptoms were improved by treatment. The LIGHT plasma concentrations correlated with IgE levels and the Severity Scoring of AD (SCORAD) index. In addition, LIGHT stimulation increased expression of CD86 and induced production of interleukin-1β in THP-1 cells. Apoptosis was inhibited, the Bcl-2 level increased and the caspase-3 level decreased in THP-1 cells stimulated with LIGHT, compared to unstimulated control cells. These results suggest that plasma LIGHT levels may be one of the promising biomarkers for AD.
authors.affiliation: Department of Dermatology, Kyoto Prefectural University of Medicine Graduate School of Medical Science, Kyoto, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Kotani
authors.forename: K
authors.initials: K
authors.lastname: Masuda
authors.forename: R
authors.initials: R
authors.lastname: Tamagawa-Mineoka
authors.forename: T
authors.initials: T
authors.lastname: Nomiyama
authors.forename: F
authors.initials: F
authors.lastname: Soga
authors.forename: M
authors.initials: M
authors.lastname: Nin
authors.forename: J
authors.initials: J
authors.lastname: Asai
authors.forename: S
authors.initials: S
authors.lastname: Kishimoto
authors.forename: N
authors.initials: N
authors.lastname: Katoh
mesh_terms: D000328:Adult; D017209:Apoptosis / Q000187:drug effects; D051940:B7-2 Antigen / Q000235:genetics / Q000378:metabolism; D015415:Biomarkers / Q000097:blood; D045744:Cell Line, Tumor; D054414:Chemokine CCL17 / Q000097:blood; D003876:Dermatitis, Atopic / Q000097:blood* / Q000276:immunology*; D018450:Disease Progression; D004804:Eosinophils / Q000187:drug effects* / Q000473:pathology; D005260:Female; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood; D053583:Interleukin-1beta / Q000235:genetics / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000187:drug effects / Q000276:immunology; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000235:genetics / Q000378:metabolism; D053326:Tumor Necrosis Factor Ligand Superfamily Member 14 / Q000097:blood* / Q000494:pharmacology; D015854:Up-Regulation; D055815:Young Adult
chemical_list: D051940:B7-2 Antigen; D015415:Biomarkers; D054414:Chemokine CCL17; D053583:Interleukin-1beta; D019253:Proto-Oncogene Proteins c-bcl-2; D053326:Tumor Necrosis Factor Ligand Superfamily Member 14; D007073:Immunoglobulin E