Inflammasome Activation Characterizes Lesional Skin of Folliculitis Decalvans

Abstract

Folliculitis decalvans (FD) is a chronic inflammatory disease leading to scarring alopecia with poorly defined pathogenesis. The aim of this study was to investigate the expression of markers associated with the activation of innate immune signals, such as inflammasome (NALP1 and NALP3), interleukin (IL)-1β and IL-8 and type I interferon (MxA). A retrospective monocentric study was conducted and included 17 patients with FD with available biopsies. Disease activity (stable vs. active) was defined clinically and histologically. Immunostaining was performed using antibodies directed against NALP1, NALP3, IL-1β, IL-8, and MxA on FD skin biopsies. Results were compared with normal controls and lichen planopilaris. Eleven patients had active disease and 6 had stable disease. NALP1, NALP3, and IL-1β expression were significantly increased in hair follicles in FD compared with controls and lichen planopilaris. This study highlights the predominant immune signal associated with inflammasome activation in FD, suggesting the use of IL-1β blockade in FD.

Efficacy and Safety of Tumour Necrosis Factor-α Antagonists for Folliculitis Decalvans: A Retrospective Case-series Pilot Study

“…The clinical response was considered good to excellent when an FD-IGA score ≤ 2 was obtained. This cut-off corresponds to the absence of pustules and/or crusts, which are considered the classical signs of disease activity ( 5 , 9 , 10 ).…”

“…This follicular dysbiosis could result from a break in the epidermal barrier, leading to subepidermal colonization by Staphylococcus aureus ( 4 ). Recently, we found involvement of the innate immune response in FD through the inflammasome and interleukin (IL)-1β signalling pathway ( 5 ). Other studies suggest that the Th17 immune response is involved in FD ( 3 ), associated with local expression of pro-inflammatory mediators, such as TNFα ( 6 ).…”

Successful treatment of refractory folliculitis decalvans with apremilast

“…Gradually, fibroblast growth factor and transforming growth factor beta also become upregulated and are thought to mediate the scarring reaction. [3][4][5] Apremilast, as a specific phosphodiesterase 4 inhibitor, suppresses innate and adaptive immune cells, including neutrophils and T cells. Reduced generation of spontaneous reactive oxygen species and of neutrophilic extracellular traps was observed in rheumatoid arthritis patients treated with apremilast.…”

Downregulation of integrin‐αvβ6 on keratinocytes in the scar of lichen planopilaris and folliculitis decalvans: Relevance for the disappearance of epidermal Langerhans cells

“…Indeed, it has been reported that the expression of IL-1b was upregulated in both LPP and FD, and the expression of type I IFN-inducible antiviral protein, myxovirus-resistance protein A, was also upregulated in LPP compared with healthy controls. 12 However, abundance of IL-1b and IFN-a is not specific in skin inflammation of LPP and FD, because IL-1b is a common inflammatory cytokine and IFN-a is primarily produced by the plasmacytoid dendritic cells which are common in the inflamed skin. Thus, it may be difficult to attribute the cause of downregulation of ITG-avb6 in LPP and FD scar and subsequent LC loss only to the effect of IL-1b and IFN-a.…”