Abstract
Ultraviolet A (UVA) irradiation is effectively used to treat patients with atopic dermatitis and other T cell mediated, inflammatory skin diseases. In the present study, successful phototherapy of atopic dermatitis was found to result from UVA radiation-induced apoptosis in skin-infiltrating T helper cells, leading to T cell depletion from eczematous skin. In vitro, UVA radiation-induced human T helper cell apoptosis was mediated through the FAS/FAS-ligand system, which was activated in irradiated T cells as a consequence of singlet oxygen generation. These studies demonstrate that singlet oxygen is a potent trigger for the induction of human T cell apoptosis. They also identify singlet oxygen generation as a fundamental mechanism of action operative in phototherapy.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Antibodies, Blocking / pharmacology
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Apoptosis / drug effects
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Apoptosis / immunology*
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Apoptosis / radiation effects*
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Dermatitis, Atopic / immunology
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Dermatitis, Atopic / radiotherapy
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Deuterium / pharmacology
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Fas Ligand Protein
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Humans
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Ligands
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Membrane Glycoproteins / biosynthesis
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Membrane Glycoproteins / radiation effects
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Naphthols / pharmacology
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Oxygen / pharmacology*
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Singlet Oxygen
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Sodium Azide / pharmacology
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T-Lymphocytes, Helper-Inducer / drug effects
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T-Lymphocytes, Helper-Inducer / immunology*
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T-Lymphocytes, Helper-Inducer / radiation effects*
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Ultraviolet Therapy*
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fas Receptor / immunology
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fas Receptor / metabolism
Substances
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Antibodies, Blocking
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FASLG protein, human
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Fas Ligand Protein
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Ligands
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Membrane Glycoproteins
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Naphthols
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fas Receptor
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Singlet Oxygen
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Sodium Azide
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3,3'-(1,4-naphthylidene)diproprionate
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Deuterium
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Oxygen