Interleukin‐32 is highly expressed in lesions of hidradenitis suppurativa

Abstract

Our findings suggest that IL-32 is overexpressed in HS. Targeting IL-32 may therefore represent a new therapeutic option for the treatment of this recalcitrant disease.

Elevated levels of the antimicrobial peptide LL‐37 in hidradenitis suppurativa are associated with a Th1/Th17 immune response

“…To this end, we investigated the expression of LL‐37 and CAMP in HS, PS, AD and healthy skin by immunohistochemistry and semi‐quantitative real‐time PCR and compared whether LL‐37 peptide and CAMP mRNA levels correlate with lesional HS skin. In addition, we examined what kind of cells (T cells, macrophages and neutrophils) and cytokines (IFN‐γ, IL‐17, IL‐23, IL‐32, IL‐1β, TNF‐α and IL‐10), which are known to be elevated in HS correlate with the presence of LL‐37. To complete our analysis, we investigated the impact of LL‐37 on the proliferation of lectin‐stimulated CD4 + and CD8 + T cells isolated from the blood of healthy donors and patients with HS and delineated by calcium assay, how LL‐37 impacts proliferation of T cells directly.…”

Interleukin-32 promotes detachment and activation of human Langerhans cells in a human skin explant model

“…Although the γ and β isoforms have been associated with anti‐inflammatory functions including reduced cell activation and proliferation, cytotoxic function and increased IL‐10 production, the majority of studies define a proinflammatory character for IL‐32 . Finally, IL‐32 has been proposed as a biomarker of skin inflammation in AD, alopecia areata and hidradenitis suppurativa . The analysis of IL‐32 isoforms mRNA expression in skin biopsies from three skin disorders (hidradenitis suppurativa, psoriasis and AD) compared with skin from healthy donors, revealed that all main IL‐32 isoforms are expressed in skin, but at different levels depending on the origin of skin disorder .…”

“…IL-32 production in the skin has been observed in inflammatory skin disorders such as AD, alopecia areata and hidradenitis suppurativa, suggesting that IL-32 production plays a critical role in skin diseases. 10,11,26 To improve the understanding of molecular mechanisms that allow LC activation in the epidermal layers, we have investigated the role of IL-32 in the epidermis. We first showed that KCs are the major cell population that produces IL-32 in the skin.…”

“…Skin barrier disruption provokes the local production of proinflammatory cytokines and chemokines by KCs, bridging innate immunity to adaptive immunity via LCs . In this regard, the production of cytokines and chemokines by KCs and LCs has been observed in many skin disorders and more particularly, the production of interleukin (IL)‐32, a proinflammatory cytokine produced by KCs . However, the impact of local production of IL‐32 on LCs has not been explored.…”

“…4,5 In this regard, the production of cytokines and chemokines by KCs and LCs has been observed in many skin disorders [6][7][8][9] and more particularly, the production of interleukin (IL)-32, a proinflammatory cytokine produced by KCs. 10,11 However, the impact of local production of IL-32 on LCs has not been explored. Here, we questioned whether IL-32 produced by KCs could impact the behaviour of LCs during microbial insults.…”