Hidradenitis suppurativa (HS) is a chronic, inflammatory, debilitating, follicular disease of the skin. Despite a high prevalence in the general population, the physiopathology of HS remains poorly understood. The use of antibiotics and immunosuppressive agents for therapy suggests a deregulated immune response to microflora. Using cellular and gene expression analyses, we found an increased number of infiltrating CD4(+) T cells secreting IL-17 and IFN-γ in perilesional and lesional skin of patients with HS. By contrast, IL-22-secreting CD4(+) T cells are not enriched in HS lesions contrasting with increased number of those cells in the blood of patients with HS. We showed that keratinocytes isolated from hair follicles of patients with HS secreted significantly more IL-1β, IP-10, and chemokine (C-C motif) ligand 5 (RANTES) either constitutively or on pattern recognition receptor stimulations. In addition, they displayed a distinct pattern of antimicrobial peptide production. These findings point out a functional defect of keratinocytes in HS leading to a balance prone to inflammatory responses. This is likely to favor a permissive environment for bacterial infections and chronic inflammation characterizing clinical outcomes in patients with HS.

At a Glance Commentary: Scientific knowledge on the Subject: severe SARS-CoV-2 infections leading to the Coronavirus disease 2019 (COVID-19) and the acute respiratory distress syndrome (ARDS) are associated with high mortality and prolonged durations of intensive care unit stay. Profound lymphopenia and elevated serum levels of pro-inflammatory cytokines, also characterized as cytokine storm, have been associated with clinical severity. However, few data compared the immunopathology of COVID-19 ARDS to that of non-COVID-19 ARDS, so that specific traits of the immune responses to severe SARS-CoV-2 infections have not been well identified. What This Study Adds to the Field: COVID-19 ARDS patients showed a phenotype of impaired adaptive immune response with profound lymphopenia and impaired/delayed lymphocyte activation. We also report a "chemokine signature" with increased serum concentrations of IP-10 and GM-CSF in COVID-19 patients. Serum concentrations of IP-10 and GM-CSF and nasopharyngeal viral loads were associated with outcomes in COVID-19 patients. Such results highlight the contribution of myeloid cells and impaired adaptive immune