Hidradenitis suppurativa (HS) is an inflammatory disease of the skin with a chronic, relapsing-remitting course. The pathogenesis of the disease is poorly understood and involves multiple factors, including genetics, environment, host-microbe interactions, and immune dysregulation. In particular, the composition of the cutaneous microbiome shifts as the disease progresses, although it is unclear whether this is a primary or secondary process. Trials with immunomodulatory therapy elucidate the role of specific immune pathways and cytokine signaling in disease mechanism, such as TNF-α, IL-1β, IL-12, IL-17, IL-23, and complement. Future studies should continue examining the causes of and contributing factors to microbial changes and immune dysregulation in HS pathogenesis.
Keywords: AMP, antimicrobial peptide; BD, β-defensin; BMI, body mass index; DC, dendritic cell; DCD, dermcidin; GSC, γ-secretase complex; HS, hidradenitis suppurativa; HiSCR, hidradenitis suppurativa clinical response; IBD, inflammatory bowel disease; IHS4, International Hidradenitis Suppurativa Severity Score System; KC, keratinocyte; MMP, matrix metalloproteinase; NET, neutrophil extracellular traps; NMSC, nonmelanoma skin cancer; PG, pyoderma gangrenosum; RCT, randomized controlled trial; SAPHO, synovitis, acne, pustulosis, hyperostosis, and osteitis; TLR, toll-like receptor; Th, T helper type; iNOS, inducible nitric oxide synthase; pDC, plasmacytoid dendritic cell.
© 2021 The Authors.