Abstract
To investigate whether specific markers for innate immunity would diminish with successful treatment in psoriasis, we analyzed lesional and non-lesional skin biopsies taken from patients with moderate to severe psoriasis during 12 weeks of treatment with etanercept in correlation with the clinical response. In the clinical responders (PASI reduction >50%), all markers (CD3, CD68, CD161, elastase, BDCA-2, TNF-alpha) showed a decline during treatment, indicating a pivotal role for innate immunity in the pathogenesis of psoriasis.
MeSH terms
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Adult
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Anti-Inflammatory Agents, Non-Steroidal / therapeutic use*
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Antigens, CD / metabolism
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Antigens, Differentiation, Myelomonocytic / metabolism
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Biomarkers / metabolism
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Biopsy
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CD3 Complex / metabolism
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Etanercept
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Female
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Humans
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Immunity, Innate*
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Immunoglobulin G / therapeutic use*
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Lectins, C-Type / metabolism
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Male
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Membrane Glycoproteins / metabolism
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Middle Aged
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NK Cell Lectin-Like Receptor Subfamily B / metabolism
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Pancreatic Elastase / metabolism
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Psoriasis / drug therapy*
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Psoriasis / metabolism
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Psoriasis / pathology*
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Receptors, Immunologic / metabolism
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Receptors, Tumor Necrosis Factor / therapeutic use*
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Skin / metabolism
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Skin / pathology*
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Tumor Necrosis Factor-alpha / metabolism
Substances
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Anti-Inflammatory Agents, Non-Steroidal
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Antigens, CD
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Antigens, Differentiation, Myelomonocytic
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Biomarkers
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CD3 Complex
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CD68 antigen, human
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CLEC4C protein, human
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Immunoglobulin G
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Lectins, C-Type
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Membrane Glycoproteins
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NK Cell Lectin-Like Receptor Subfamily B
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Receptors, Immunologic
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Receptors, Tumor Necrosis Factor
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Tumor Necrosis Factor-alpha
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Pancreatic Elastase
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Etanercept