cells Review Hidradenitis Suppurativa: Where We Are and Where We Are Going Emanuele Scala 1,* , Sara Cacciapuoti 2 , Natalie Garzorz-Stark 1,3, Matteo Megna 2 , Claudio Marasca 2, Peter Seiringer 1,4, Thomas Volz 3, Kilian Eyerich 1,3,5,† and Gabriella Fabbrocini 2,† 1 Division of Dermatology and Venereology, Department of Medicine Solna and Center for Molecular Medicine, Karolinska Institutet, 17176 Stockholm, Sweden;
[email protected] (N.G.-S.);
[email protected] (P.S.);
[email protected] (K.E.) 2 Department of Clinical Medicine and Surgery, University of Naples Federico II, 80131 Naples, Italy;
[email protected] (S.C.);
[email protected] (M.M.);
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[email protected] (G.F.) 3 Department of Dermatology and Allergy, Technical University of Munich, 80802 Munich, Germany;
[email protected] 4 Center for Allergy and Environment, Technical University, Helmholtz Center Munich, 80802 Munich, Germany 5 Unit of Dermatology, Department of Dermatology and Venereology, Karolinska University Hospital, 17176 Stockholm, Sweden * Correspondence:
[email protected] † These authors contributed equally to the manuscript. Abstract: Hidradenitis suppurativa (HS) is a chronic inflammatory skin disease primarily affecting apocrine gland-rich areas of the body. It is a multifactorial disease in which genetic and environmental factors play a key role. The primary defect in HS pathophysiology involves follicular occlusion Citation: Scala, E.; Cacciapuoti, S.; of the folliculopilosebaceous unit, followed by follicular rupture and immune responses. Innate Garzorz-Stark, N.; Megna, M.; pro-inflammatory cytokines (e.g., IL-1β, and TNF-α); mediators of activated T helper (Th)1 and Th17 Marasca, C.; Seiringer, P.; Volz, T.; cells (e.g., IFN-γ, and IL-17); and effector mechanisms of neutrophilic granulocytes, macrophages, Eyerich, K.; Fabbrocini, G.