Hidradenitis suppurativa (HS) is a chronic inflammatory skin disease characterized by recurrent inflammatory lesions, which affect skin and hair follicles in intertriginous areas. HS has a multifactorial aetiology resulting in barrier dysfunction associated with aberrant immune activation. There is increased evidence for the role of inflammasomes in the pathophysiology of inflammatory skin diseases, including HS. Inflammasomes are multiprotein complexes activated following exposure to danger signals, including microbial ligands and components of damaged host cells. Inflammasome activation induces many signalling cascades and subsequent cleavage of proinflammatory cytokines - most notably interleukin (IL)-1β - which have a role in HS pathogenesis. Limited immunotherapies are approved for treating moderate-to-severe HS, with variable response rates influenced by disease heterogeneity. Inflammasomes represent attractive targets to suppress multiple inflammatory pathways in HS, including IL-1β and IL-17. This review aims to summarize the role of inflammasomes in HS and to evaluate evidence for inflammasomes as therapeutic targets for HS treatment.
Hidradenitis suppurativa, or ‘HS’ for short, is a skin condition that causes recurrent lesions on the body. Evidence suggests that a type of molecular structure called an ‘inflammasome’ could play a role in HS. Inflammasomes are found in immune cells and skin cells. They control the release of key immune molecules called ‘cytokines’. Cytokines help to produce effective immune responses. In HS, inflammasomes are thought to be out of control and lead to the over-production of cytokines. Excessive levels of a cytokine called ‘interleukin-1beta’ have been found in people with HS. In this review, we bring together evidence on the role of inflammasomes in HS. Our research suggests that using drugs to target inflammasomes could be an effective way to treat people with HS.
© The Author(s) 2024. Published by Oxford University Press on behalf of British Association of Dermatologists.