Background Pemphigus is an autoimmune disease characterized by intraepiderm
al blisters induced by pemphigus IgG. In addition to autoantibodies, molecu
lar mechanisms involved in acantholysis remain largely unknown. For this re
ason. we address a possible role of the inflammatory cytokines IL-6 and TNF
alpha in pemphigus lesions.
Methods Sixteen biopsies from patients with different types of pemphigus we
re studied by in situ hybridization using DNA fluorescent probes for IL-6 a
nd TNF alpha mRNA.
Results Fifty-six percent of lesional biopsies exhibited cytokine gene expr
ession, which was poorly expressed in noninvolved skin. Deposits of TNF alp
ha 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.