Document Detail


Increased plasma LIGHT levels in patients with atopic dermatitis.
MedLine Citation:
PMID:  22519595     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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:
H Kotani; K Masuda; R Tamagawa-Mineoka; T Nomiyama; F Soga; M Nin; J Asai; S Kishimoto; N Katoh
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Clinical and experimental immunology     Volume:  168     ISSN:  1365-2249     ISO Abbreviation:  Clin. Exp. Immunol.     Publication Date:  2012 Jun 
Date Detail:
Created Date:  2012-04-23     Completed Date:  2012-06-20     Revised Date:  2013-06-26    
Medline Journal Info:
Nlm Unique ID:  0057202     Medline TA:  Clin Exp Immunol     Country:  England    
Other Details:
Languages:  eng     Pagination:  318-24     Citation Subset:  IM    
Copyright Information:
© 2012 The Authors. Clinical and Experimental Immunology © 2012 British Society for Immunology.
Affiliation:
Department of Dermatology, Kyoto Prefectural University of Medicine Graduate School of Medical Science, Kyoto, Japan.
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MeSH Terms
Descriptor/Qualifier:
Adult
Antigens, CD86 / genetics,  metabolism
Apoptosis / drug effects
Biological Markers / blood
Cell Line, Tumor
Chemokine CCL17 / blood
Dermatitis, Atopic / blood*,  immunology*
Disease Progression
Eosinophils / drug effects*,  pathology
Female
Humans
Immunoglobulin E / blood
Interleukin-1beta / genetics,  metabolism
Male
Middle Aged
Monocytes / drug effects,  immunology
Proto-Oncogene Proteins c-bcl-2 / genetics,  metabolism
Tumor Necrosis Factor Ligand Superfamily Member 14 / blood*,  pharmacology
Up-Regulation
Young Adult
Chemical
Reg. No./Substance:
0/Antigens, CD86; 0/Biological Markers; 0/Chemokine CCL17; 0/Interleukin-1beta; 0/Proto-Oncogene Proteins c-bcl-2; 0/Tumor Necrosis Factor Ligand Superfamily Member 14; 37341-29-0/Immunoglobulin E
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