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TNFα and IL‐6 are mediators in the blistering process of pemphigus
Author(s) -
LópezRobles Eréndira,
AvalosDíaz Esperanza,
VegaMemije Elisa,
HojyoTomoka Teresa,
Villalobos Ricardo,
Fraire Saúl,
DomíguezSoto Luciano,
HerreraEsparza Rafael
Publication year - 2001
Publication title -
international journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.677
H-Index - 93
eISSN - 1365-4632
pISSN - 0011-9059
DOI - 10.1046/j.1365-4362.2001.01083.x
Subject(s) - pemphigus , acantholysis , medicine , cytokine , autoantibody , immunology , autoimmune disease , paraneoplastic pemphigus , immunopathology , tumor necrosis factor alpha , mediator , pemphigus vulgaris , in situ hybridization , pathology , messenger rna , gene , biology , antibody , endocrinology , biochemistry
Background Pemphigus is an autoimmune disease characterized by intraepidermal blisters induced by pemphigus IgG. In addition to autoantibodies, molecular mechanisms involved in acantholysis remain largely unknown. For this reason, we address a possible role of the inflammatory cytokines IL‐6 and TNFα in pemphigus lesions. Methods Sixteen biopsies from patients with different types of pemphigus were studied by in situ hybridization using DNA fluorescent probes for IL‐6 and TNFα mRNA. Results Fifty‐six percent of lesional biopsies exhibited cytokine gene expression, which was poorly expressed in noninvolved skin. Deposits of TNFα and IL‐6 were products of in situ transcription at the epidermal level. Conclusions Inflammatory cytokine expression around the blister could play a mediator role in pemphigus lesions by increasing epithelial damage.