Apocrine Gland–Rich Skin Has a Non-Inflammatory IL-17–Related Immune Milieu, that Turns to Inflammatory IL-17–Mediated Disease in Hidradenitis Suppurativa

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The pathogenesis of hidradenitis suppurativa/acne inversa (HS) is still unclear, but is likely initiated by follicular occlusion of the pilosebaceous-apocrine units (Hoffman et al., 2017) in the apocrine gland-rich (AGR) skin (armpits, intramammary fold, genital groin, perianal areas, and buttocks). The outstanding role of keratinocytes in the initiation phase was also highlighted by recently described signaling pathways (Notch and mTOR signaling, IL-36 pathway) related to HS pathophysiology (Balato et al., 2019; Di Caprio et al., 2017; Scala et al., 2018).