SummaryBackground There is a dearth of information on the precise pathogenesis of hidradenitis suppurativa (HS), but immune dysregulation is implicated. Objectives To determine the nature of the immune response in HS. Methods Skin biopsies -lesional, perilesional (2 cm away) and uninvolved (10 cm away) -were obtained from patients with HS and healthy controls. The expression of various cytokines was determined by enzyme-linked immunosorbent assay, flow cytometry and real-time polymerase chain reaction. Results The expression of the inflammatory cytokines interleukin (IL)-17, IL-1b and tumour necrosis factor-a was enhanced in lesional skin of patients with HS. In addition, IL17A and IL1B mRNA were enhanced in clinically normal perilesional skin. CD4 + T cells produced IL-17 in HS, while CD11c + CD1a À CD14

Summary Background Human skin is populated by diverse bacteria and there is increasing evidence that resident bacteria play a key role initiating immune responses in cutaneous diseases such as atopic dermatitis, psoriasis and hidradenitis suppurativa. Bacteria are present at all layers of the skin but many studies have relied on swabs to profile the skin microbiota. Objectives As the pathogenesis of many skin conditions is dermal, we wanted to compare the microbiota obtained in swabs (surface) and biopsies (dermis). Methods Using 16S rRNA gene sequencing we established the microbial profiles of skin swabs and skin biopsies in 16 patients. Results We found differences in both diversity and taxonomic composition of the microbiome obtained from swabs and biopsies of the same individual. Several taxa were found to be more abundant in the swabs, which displayed significantly higher community richness, but Clostridiales and Bacteroidetes were significantly enriched in the biopsies. Most published research on cutaneous microbiota has been based on skin swabs, which represent the surface of the skin. Conclusions Our study demonstrated a clear difference between the microbiome observed from skin swabs and skin biopsies. These findings may be highly relevant in disorders such as psoriasis where pathogenesis arises in the dermis. What's already known about this topic? 16S RNA gene sequencing has facilitated study of the skin microbiome. Several studies have sequenced the microbiome sampled by skin swabs. What does this study add? The microbiome data obtained using swabs and biopsies were different. Diseases that are predominantly dermal should be studied using both swabs and biopsies.

Our data show that one-third of patients with PD have autoantibodies to Col XVII that also bind to TH þ neurons. The lack of reactivity of PD autoantibodies with skin suggests the autoantibodies develop from neuronal Col XVII. The subset of patients with neurologic disease that develop BP likely result from epitope spreading to regions of Col XVII that are pathogenic in skin. A key question that remains is whether Col XVII autoantibodies have a detrimental effect on PD or are otherwise predictive of disease onset/outcomes. Finally, these data suggest loss of tolerance to neuronal Col XVII may contribute to the risk for pemphigoid.