Abstract
One of the most frustrating aspects of treating psoriasis is the tendency of psoriatic skin lesions to recur after therapy has been discontinued. Not only do lesions recur, but they often recur in the same anatomical locations, expanding to the size they were before therapy. This engenders feelings of frustration and futility in both patients and the dermatologists who care for them. In this issue, Suárez-Fariñas and colleagues identified a gene set-the residual disease genomic profile-of psoriasis, suggesting the presence of both immunologic and structural abnormalities within healed psoriatic lesions. By understanding this "invisible lesion," we may be one step closer to curing psoriasis.
Publication types
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Comment
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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CD8-Positive T-Lymphocytes / immunology*
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CD8-Positive T-Lymphocytes / metabolism
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CD8-Positive T-Lymphocytes / pathology*
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Etanercept
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Humans
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Immunoglobulin G / therapeutic use
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Interleukin-17 / genetics
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Interleukin-17 / metabolism
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Lymphotoxin-alpha / genetics
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Lymphotoxin-alpha / metabolism
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Psoriasis / drug therapy
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Psoriasis / genetics*
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Psoriasis / pathology*
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Receptors, Antigen, T-Cell, alpha-beta / genetics
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Receptors, Antigen, T-Cell, alpha-beta / metabolism
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Receptors, Tumor Necrosis Factor / therapeutic use
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Recurrence
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Skin / immunology*
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Skin / metabolism
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Skin / pathology*
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Tumor Necrosis Factor-alpha / antagonists & inhibitors
Substances
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Immunoglobulin G
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Interleukin-17
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Lymphotoxin-alpha
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Receptors, Antigen, T-Cell, alpha-beta
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Receptors, Tumor Necrosis Factor
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Tumor Necrosis Factor-alpha
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Etanercept