Abstract
We have recently shown that skin lesions of the autoimmune disease pemphigus vulgaris are associated with Fas-mediated apoptosis. Here, we describe the induction of the Fas-dependent apoptosis pathway in cultured keratinocytes by pemphigus vulgaris autoantibodies (PV-IgG), as seen from a variety of cellular, morphological and biochemical parameters. All apoptotic characters appear stronger and faster in aged cultures than in young, showing increased susceptibility of senescent keratinocytes to PV-IgG-mediated apoptotic death and culture lesions. Together with immunosenescence, this phenomenon may explain the late onset of pemphigus disease.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Apoptosis / immunology*
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Autoantibodies / immunology*
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Caspase Inhibitors
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Caspases / biosynthesis
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Cells, Cultured
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Cellular Senescence / physiology*
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Cysteine Proteinase Inhibitors / pharmacology
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DNA Fragmentation
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Fas Ligand Protein
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Humans
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Immunoglobulin G / immunology
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Keratinocytes / cytology*
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Keratinocytes / immunology*
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Keratinocytes / metabolism
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Membrane Glycoproteins / biosynthesis
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Membrane Glycoproteins / immunology
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Pemphigus / immunology*
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Proto-Oncogene Proteins c-bcl-2 / metabolism
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Tumor Suppressor Protein p53 / metabolism
Substances
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Autoantibodies
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Caspase Inhibitors
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Cysteine Proteinase Inhibitors
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FASLG protein, human
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Fas Ligand Protein
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Immunoglobulin G
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Membrane Glycoproteins
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Proto-Oncogene Proteins c-bcl-2
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Tumor Suppressor Protein p53
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Caspases