Table 1.
Hidradenitis suppurativa skin transcriptome.
Fig 1.
CIBERSORT analysis of HS skin transcriptome.
(A) Heatmap showing normalized absolute abundance for each cell type in individual samples, mean abundance for each cell type is also displayed (left, green); (B) bar graph showing absolute abundance of each cell type in non-lesional (NL) and lesional (LS) samples; and (C) mean abundance of each cell type in all NL samples (left) and LS samples (right). Data from S4 Table. The abundance of plasma cells was significantly higher in LS versus NL skin (*FDR <0.05).
Table 2.
Hidradenitis suppurativa blood proteome.
Fig 2.
Dysregulation of complement pathway components.
Fold change of skin DEGs (S4 Table) (blue arrows) and blood DEPs (Table 1) (red arrows) in the context of the complement cascade. It is not entirely clear which of the three complement activation pathways is engaged in HS, classical, lectin or alternative pathways. However, the classical pathway may be primarily implicated because of the involvement of C4 and the presence of immunoglobulins in the skin and blood. Additionally, lectin pathway activators, such as MBL and MASP, were not identified as DEGs in the skin or DEPs in the serum. Reprinted from Springe Nature under a CC BY license, with permission from Springe Nature, original copyright 2008. Modified by permission from Springer Customer Service Center GmbH: Springer Nature, Clinical and Basic Immunodermatology by Gaspari and Tyring, COPYRIGHT (2008).
Fig 3.
Proposed pathogenesis of hidradenitis suppurativa.
Pathogenesis of hidradenitis suppurativa (HS) can be considered in two phases, initiation and progression. Our analysis of advanced HS showed immunoglobulin (Igs) transcripts, antimicrobial peptides (AMPs), an interferon signature, plasma cells in lesional skin, and an association with complement dysregulation. Considered in the context of prior findings in HS such as numerous neutrophils, B cells, plasma cells, TLR2, and IL-32, there appears to be a concerted immune response (IR) to eradicate bacteria in HS. These efforts may drive HS disease progression. There are also data supporting general cutaneous immune responses such as abundant AMPs, pro-inflammatory cytokines including IL-1, IL-6, IL-17, IL-12/23, and a dysregulated Th17/T-reg cell axis (often seen in other chronic skin diseases such as psoriasis or atopic dermatitis).