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Pemphigus vulgaris autoantibodies induce apoptosis in HaCaT keratinocytes
Author(s) -
Pelacho B.,
Natal C.,
España A.,
Sánchez-Carpintero I.,
Iraburu M.J.,
López-Zabalza M.J.
Publication year - 2004
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2004.03.107
Subject(s) - hacat , autoantibody , desmoglein 3 , pemphigus vulgaris , desmoglein , keratinocyte , immunology , antibody , apoptosis , pemphigus , desmosome , mucocutaneous zone , chemistry , medicine , microbiology and biotechnology , biology , cell , pathology , disease , in vitro , biochemistry
Pemphigus vulgaris (PV) is an autoimmune disease characterized by binding of IgG autoantibodies to epidermal keratinocyte desmosomes. IgG autoantibodies obtained from a patient with mucocutaneous PV reacted with plakoglobin (Plkg) in addition to desmoglein‐3 (Dsg3) and Dsg1. Immunofluorescence analysis confirmed that IgG autoantibodies, unlike antibodies from a healthy volunteer, caused disruption of cell–cell contacts in HaCaT keratinocytes. Moreover, apoptosis was enhanced in cells treated with autoantibodies compared to those treated with normal antibodies. The apoptotic process induced by IgG autoantibodies was characterized by caspase‐3 activation, Bcl‐2 depletion and Bax expression. The present report demonstrates that PV IgG autoantibodies promote apoptosis in HaCaT keratinocytes.