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 TNFalpha 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 TNFalpha mRNA.
Results: Fifty-six percent of lesional biopsies exhibited cytokine gene expression, which was poorly expressed in noninvolved skin. Deposits of TNFalpha 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.