The pathogenesis of hidradenitis suppurativa/acne inversa (HS) is still unclear, but is likely initiated by follicular occlusion of the pilosebaceousapocrine 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). Following keratinocyte activation, proliferation and follicular occlusion, immune cell infiltration, pro-inflammatory cytokine, and chemokine and antimicrobial peptide (AMP) production resulting in severe destruction of the surrounding tissue lead to fully developed immunemediated inflammation. In HS, IL-17 levels have been shown to be elevated (Schlapbach et al., 2011; Wolk et al., 2011) and IL-17 was proven to be produced mainly by inflammatory T helper 17 type lymphocytes (Kelly et al., 2015; Schlapbach et al., 2011). IL-17 is a multifaceted cytokine that has both physiological and pathological, or in another classification non-inflammatory and inflammatory, roles at least on three different levels: i) During homeostatic conditions, it has a role in maintaining immune surveillance of barriers that cooperate with commensals; ii) it can also protect barrier surfaces during the invasion of extracellular pathogens; whereas iii) it appears to be one of the most prominent factors in the initiation and maintenance of autoimmunity and chronic inflammation (Abusleme and Moutsopoulos, 2017). In our previous studies (Beke et al., 2018; Dajnoki et al., 2017), we reported that sebaceous glanderich skin areas, considered as oily skin, similarly to the previously published topographical distinctions of the microbiota and the chemical milieu (Bouslimani et al., 2015; Grice and Segre, 2011), are equipped with a significantly different immune and barrier supply compared to sebaceous gland-poor areas, considered as dry skin. In the present project, we aimed to further analyze whether AGR areas (as analogous to moist skin in previous literature) also develop their characteristic immune and barrier milieu because these skin regions were proven to possess specific microbiota composition, chemical milieu, moisture content, and temperature appreciably different from apocrine gland-poor (AGP) skin (AGP skin biopsies were taken also from dry skin, similarly to previous sebaceous gland-poor biopsies, containing neither apocrine nor sebaceous glands, detailed identification in Supplementary Table S1 online)(Grice and Segre, 2011). We were interested in whether AGR skin’s immune characteristics could predispose this region to develop specifically an IL-17-mediated inflammation, and also aimed to search for the downstream tissue effects of IL-17 in HS, because a systematic survey was missing. Biopsies from axillary region (representing moist AGR skin, n= 8) and from shin and arm areas (representing dry AGP skin, n= 8) of healthy individuals and lesional axillary skin of HS patients (n= 8) were gained (Supplementary Table S1), after obtaining written informed consent, according to the Declaration of Helsinki principles, and analyzed by quantitative real-time PCR and immunohistochemistry(IHC), which was quantified by Panoramic Viewer software (3DHISTECH, Budapest, Hungary) after whole slide imaging. First, dendritic cell (DC) and T-cell characteristics of AGR were compared to AGP, then HS to AGR. The study was approved by the local ethics committee of University of Debrecen, Hungary. IHC revealed significantly elevated …