Serum biomarker profiles suggest that atopic dermatitis is a systemic disease
The component loadings showed that principal component 1 (explaining 23% of variability) is primarily driven by IL-5, IL-1β, IL-7, IL-1R1, and IL-15; principal component 2 (explaining 12% of variability) by IFN-β, IL-20, IL-1Rα, TNF-β, and monocyte chemoattractant protein-3 (MCP-3); and principal co...
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Published in | Journal of allergy and clinical immunology Vol. 141; no. 4; pp. 1523 - 1526 |
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Main Authors | , , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Elsevier Inc
01.04.2018
Elsevier Limited |
Subjects | |
Online Access | Get full text |
ISSN | 0091-6749 1097-6825 1097-6825 |
DOI | 10.1016/j.jaci.2017.12.991 |
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Summary: | The component loadings showed that principal component 1 (explaining 23% of variability) is primarily driven by IL-5, IL-1β, IL-7, IL-1R1, and IL-15; principal component 2 (explaining 12% of variability) by IFN-β, IL-20, IL-1Rα, TNF-β, and monocyte chemoattractant protein-3 (MCP-3); and principal component 3 (explaining 6% of the variation) by tissue inhibitor of metalloproteinase 1, cathepsin-S, intercellular adhesion molecule 1, pulmonary and activation-regulated chemokine, and angiotensin-converting enzyme (ACE). Associations among AD, cardiovascular risk factors, and CVD have been reported in several population-based studies from North America and Asia.1 However, recent publications from Europe found no association or only an association between severe AD and CVD.2-4 The association between adult AD and CVD would be consistent with a recent study that showed the occurrence of severe CVD and metabolic abnormalities in a mouse model of severe dermatitis resulting from persistent release of IL-1 family cytokines from the skin.5 Interestingly, both skin and systemic pathologies were ameliorated by treatment with anti–IL-1α and anti–IL-1β neutralizing antibodies. [...]we have shown that biomarker expression profiles in moderate-to-severe AD patients are clearly different from those in healthy controls, which confirms the presence of systemic inflammation in AD patients and supports the hypothesis that AD is a systemic disorder. |
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Bibliography: | SourceType-Scholarly Journals-1 ObjectType-Correspondence-2 content type line 14 ObjectType-Letter to the Editor-1 ObjectType-Article-2 ObjectType-Correspondence-1 content type line 23 |
ISSN: | 0091-6749 1097-6825 1097-6825 |
DOI: | 10.1016/j.jaci.2017.12.991 |