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. 2022 Jul 28;13:960488. doi: 10.3389/fimmu.2022.960488

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Copyright © 2022 Chopra, Arens, Amornpairoj, Lowes, Tomic-Canic, Strbo, Lev-Tov and Pastar

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Proposed pathways of AMPs and complement deregulation in HS. Follicular inflammation, microbial dysbiosis and biofilm stimulate keratinocytes to overexpress LL-37 (cathelicidin), S100A7, S100A8/A9, hBD-2, and hBD-3. Immunomodulatory function of these AMPs includes chemotaxis of macrophages, monocytes, neutrophils, T cells, and dendritic cells (DC) and production of cytokines. Complement pathways are hyperactivated in HS causing elevated C5a and C9 levels. Constitutive production of hBD-1 from keratinocytes and DCD production from eccrine sweat glands is inhibited in HS skin which may result in microbial dysbiosis. Overall, these events lead to a persistent vicious cycle of chronic inflammation, which is ineffective in eliminating pathogens and biofilms.