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. 2021 May 15;22(5-6):276–288. doi: 10.1038/s41435-021-00133-9

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — Diverse microbes on the skin surface and hair follicles interact with each other such that they limit the proliferation of pathogenic organisms. Microbes influence the growth of other microbes via secretion of bacteriocins, auto-induced peptides (AIPs), phenol soluble modulins (PSMs) and cyclic anti-microbial peptides (AMPs). Keratinocytes inhibit microbial growth by constitutively secreting antimicrobial peptides such as cathelicidin and human beta defensins (hβDs). Pattern recognition receptors (PRRs) recognize microbial structures to induce appropriate innate immune responses. Lipotechoic acid (LTA) from Staphylococcus (S.) epidermidis is recognized via toll-like receptor 2 (TLR-2). Mucosa-associated invariant T (MAIT) cells specifically respond to microbial-derived riboflavin metabolites. Innate cells such as Langerhans cells (LCs) and dendritic cells (DCs) sample microbial antigens within the hair follicle, while secretion of chemokines including chemokine (C-C motif) ligand 20 (CCL20) control the recruitment of lymphocyte subsets. Dysbiosis is associated with overgrowth of microbes such as S. aureus, which employs clumping factor B (ClfB), toxins, proteases and superantigens to colonize the skin and induce damaging inflammatory responses. Figure created with BioRender.com.