The role of the microbiome in scalp hair follicle biology and disease

Polak-Witka, Katarzyna; Rudnicka, Lidia; Blume-Peytavi, Ulrike; Vogt, Annika

doi:10.1111/exd.13935

Cited by 83 publications

(78 citation statements)

References 86 publications

(176 reference statements)

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“…Since failure of IP mechanisms enables AA development, it is logical to anticipate that restoring and/or supplementing IP signalling is a highly effective way to treat AA and prevent future relapse. Exogenous factors could modify the nature and intensity of IP and its breakdown in AA including the HF and gut microbiomes, 326 the bioavailability of energy for immune cell activity 327 and atopic responses to environmental allergens, 264,328 for example. As such, targeting these external factors with treatment may facilitate IP regeneration in AA‐affected HFs.…”

Section: Therapeutic Perspectivesmentioning

confidence: 99%

Hair follicle immune privilege and its collapse in alopecia areata

Bertolini

McElwee

Gilhar

et al. 2020

Experimental Dermatology

143

150

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Anagen stage hair follicles (HFs) exhibit “immune privilege (IP)” from the level of the bulge downwards to the bulb. Both passive and active IP mechanisms protect HFs from physiologically undesired immune responses and limit immune surveillance. IP is relative, not absolute, and is primarily based on absent, or greatly reduced, intra‐follicular antigen presentation via MHC class I and II molecules, along with prominent expression of “no danger” signals like CD200 and the creation of an immunoinhibitory signalling milieu generated by the secretory activities of HFs. Perifollicular mast cells, Tregs and other immunocytes may also contribute to HF IP maintenance in healthy human skin. Collapse of anagen hair bulb IP is an essential prerequisite for the development of alopecia areata (AA). In AA, lesional HFs are rapidly infiltrated by NKG2D + T cells and natural killer (NK) cells, while perifollicular mast cells acquire a profoundly pro‐inflammatory phenotype and interact with autoreactive CD8+ T cells. Using animal models, significant functional evidence has accumulated that demonstrates the dominance of the immune system in AA pathogenesis. Purified CD8+T‐cell and NK cell populations alone, which secrete fγ, suffice to induce the AA phenotype, while CD4+T‐cells aggravate it, and Tregs and iNKT cells may provide relative protection against AA development. While IP collapse may be induced by exogenous agents, inherent IP deficiencies might confer increased susceptibility to AA for some individuals. Thus, a key goal for effective AA management is the re‐establishment of a functional HF IP, which will also provide superior protection from disease relapse.

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Section: Therapeutic Perspectivesmentioning

confidence: 99%

Hair follicle immune privilege and its collapse in alopecia areata

Bertolini

McElwee

Gilhar

et al. 2020

Experimental Dermatology

143

150

View full text Add to dashboard Cite

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“…It protects mammals against extreme temperatures, UV light or physical trauma. However, at the same time, the HF provides a niche for microorganisms that can challenge the immune system ( Polak-Witka et al, 2019 ). HF morphogenesis draws its origins from the interaction between the embryonic ectoderm and the underlying mesoderm and is completed two weeks after birth ( Schneider et al, 2009 ).…”

Section: Introductionmentioning

confidence: 99%

The hair cycle underlies regulation of Langerhans cell renewal

Voisin

Chartoire

Devouassoux

et al. 2019

Preprint

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In the epidermis, Langerhans cells (LCs) provide an essential link between the innate and adaptive immune systems. They self-renew in situ and continuously transport antigen from skin to lymph node (LN) T cells in the steady state. The cyclic renewal of hair follicles (HF) causes profound alterations in the cutaneous microenvironment, however little is known about its impact on LC homeostasis. Here we show that mouse LCs developed normally in the absence of hair but perceived critical transition periods in the hair cycle. LCs underwent a proliferation burst during the HF growth phase (anagen). Reinitiation or abolishment of anagen as well as loss of the HF had direct consequences on LC self-renewal. Because dividing LCs were found close to the anagen HF, we searched for the proliferative signal within this structure and identified increased Il34 expression by HF stem cells and their progeny. Inhibition of the IL-34 receptor CSF-1R at the onset of anagen completely and specifically blocked LC proliferation. Altogether, our findings demonstrate that the hair cycle directly oversees LC self-renewal and migration.

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“…Polak-Witka et al review the role of the microbiome in hair follicle biology and disease. [28] How microbes interact with the immune system and how they might elicit immune responses in the vicinity of hair follicles may be important for understanding skin and hair conditions including psoriasis, androgenetic alopecia and alopecia areata, but it is particularly relevant for understanding folliculitis decalvans (FD). Matard and colleagues reveal a persistent, abnormal subepidermal microbiota is present in FD, both in lesional skin and also in non-lesional skin.…”

Section: Sc Arring Alopeciamentioning

confidence: 99%