Intrinsic Defect in Keratinocyte Function Leads to Inflammation in Hidradenitis Suppurativa

Abstract : 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.
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Article dans une revue
Journal of Investigative Dermatology, Nature Publishing Group: Open Access Hybrid Model Option A, 2016, 136 (9), pp.1768 - 1780
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https://hal.inria.fr/hal-01406612
Contributeur : Sandrine Darmigny <>
Soumis le : jeudi 1 décembre 2016 - 13:33:20
Dernière modification le : lundi 6 novembre 2017 - 10:49:48

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  • HAL Id : hal-01406612, version 1
  • PUBMED : 27206704

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Claire Hotz, Michele Boniotto, Aurélie Guguin, Mathieu Surenaud, Francette Jean-Louis, et al.. Intrinsic Defect in Keratinocyte Function Leads to Inflammation in Hidradenitis Suppurativa. Journal of Investigative Dermatology, Nature Publishing Group: Open Access Hybrid Model Option A, 2016, 136 (9), pp.1768 - 1780. 〈hal-01406612〉

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