Targeting Neutrophil Function as Therapy for Hidradenitis Suppurativa

TL;DR

This paper explores how targeting neutrophil function could lead to better treatments for hidradenitis suppurativa, a chronic inflammatory skin disease.

Contribution

The paper highlights novel therapeutic strategies focusing on modulating neutrophil activity in hidradenitis suppurativa.

Findings

Neutrophils play a key role in the inflammation seen in hidradenitis suppurativa.

Therapies targeting neutrophil trafficking, proteases, and NETs are showing promise in clinical trials.

Current treatments like TNF-α and IL-17 inhibitors have limitations, highlighting the need for new approaches.

Abstract

Hidradenitis suppurativa (HS) is a chronic, recurrent inflammatory skin disease characterized by painful nodules, abscesses, and epithelialized tunnels, predominantly affecting flexural regions. With a global prevalence of approximately 1%, HS has a significant negative impact on quality of life. Multi-omics and histopathology studies have revealed a complex interplay between innate and adaptive immunity in HS, with neutrophils emerging as important drivers of inflammation. While therapies targeting TNF-α and IL-17 isoforms offer a degree of benefit, significant unmet need remains. Neutrophil signatures in HS lesions and the circulation underscore the rationale for selective modulation of neutrophil function. Strategies advancing through clinical trials include inhibition of chemokine-mediated trafficking, neutrophil serine protease inactivation and suppression of neutrophil extracellular traps (NETs), which amplify inflammatory and autoimmune responses. These emerging therapies mark a significant shift toward targeted neutrophil modulation, offering new opportunities to improve outcomes for patients with HS.

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