The aim of this exploratory study is to analyze the interplay between microbiota and the innate and adaptative immune response in the pathogenesis of HS. To better understand this host-microbiota interplay, we will assess the number, frequency and functional phenotypes of the different lymphocyte subsets in HS patients, with a special focus regarding the UL. In the same time, we will assess the diversity and nature of skin microbiota of the same patients. Finally, we will explore the relation between the immune response and the skin microbiota in HS, using correlation analysis (Spearman coefficient).~In this study, HS patients will be their own control for leucocyte phenotyping, cytokine analysis and T Cells Receptor (TCR) sequencing (skin biopsies) and for skin microbiota analysis. Paired (age/sex) healthy volunteers will be controls for gut microbiota analysis and for immunophenotyping of circulating leukocytes (Peripheral Blood Mononuclear Cells (PBMC) analysis).
Hidradenitis Suppurativa (HS) is a chronic disabling inflammatory skin disorder associated with the development of painful and purulent lesions of the folds (armpits, inguinal folds, sub-mammary glands). HS most often develops in adolescence or young adulthood and is characterized by inflammation of the pilo-sebaceous system, of progressive severity (folliculitis, nodule, abscess, fistula). The pathogenesis of HS is still poorly understood: the fact that patients respond to combinations of antibiotics and/or immunosuppressive treatments suggests that the disease could be due to a dysregulated immune response against microbial skin flora. Unconventional lymphocytes (UL), classically considered being at the interface of innate and adaptive immunity, play an important role in immune protection against microbial flora. But UL dysfunction has also been reported in many autoimmune diseases involving various tissues (joints, digestive tract, skin). The uncontrolled and chronic activation of these UL by skin microbiota could therefore play a role in the pathogenesis of HS.