A ?hairy? privilege

Paus, Ralf; Nickoloff, Brian J.; Ito, Taisuke

doi:10.1016/j.it.2004.09.014

Cited by 292 publications

(410 citation statements)

References 61 publications

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“…gonads -and gonadal steroids in turn influence the brain; and so do corticosteroids secreted from the adrenal gland under the influence of ACTH (Adreno Corticotropic Hormone) and regulate the human HF pigmentary unit (Ito et al, 2005; Slominski et al, Tobin and Krauser, 2005;2007;Watts, 2006). Peptides secreted by hypothalamic neuroendocrine neurons into the blood often appeared to complement with peripheral actions e.g in the HF it is believed to play a role in the pathogenesis of alopecia areata (Kim et al, 2006;Pritchard and White, 2007; Sivilia et al, 2008;Sun et al, 2007).…”

Section: Clinical Importance Of Hair Follicle Stem Cellsmentioning

confidence: 99%

“…1) of both murine and human HFs that were classified as "HF epithelial stem cells" (HFeSC) on the basis of GFP (green fluorescent protein)-visualized cytokeratin 15 promoter activity for targeting epithelial SCs in the HF bulge (Liu et al, 2003;Ito et al, 2005). Morris et al, 2004;Ohyama et al, 2006;Tiede et al, 2007 andTumbar et al, 2004, have provided particularly valuable pointers to endocrine controls of this population of HFeSCs (Tables 1 and 2).…”

Section: Pointers From Hfesc Gene Profiling Studiesmentioning

confidence: 99%

“…It had long been thought that only the anagen hair bulb epithelium is a site of relative immune privilege, where e.g. immunogenic, melanogenesis-associated autoantigens are shielded from potentially deleterious autoimmune responses, and that the collapse of this anagen hair bulb immune privilege is a critical step in the pathogenesis of the most common autoimmune hair growth disorder, alopecia areata (Gilhar et al, 2007;Paus et al, 2005).…”

Section: Neuroendocrine Controls Of Hair Follicle Immune Privilege Anmentioning

confidence: 99%

“…These also showed higher serum corticosterone levels (Aoki et al, 2003). Thus, both systemic and intracutaneous CRH levels rise in response to perceived stress, which may then induce not only higher adrenal, but also increased intrafollicular glucocorticoid synthesis (Ito et al, 2005). It is conceivable that GR-expressing HFeSC (Table.…”

mentioning

confidence: 99%

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(Neuro-)endocrinology of epithelial hair follicle stem cells

Paus

Arck

Tiede

2008

Molecular and Cellular Endocrinology

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The hair follicle is a repository of different types of somatic stem cells. However, even though the hair follicle is both a prominent target organ and a potent, non-classical site of production and/or metabolism of numerous polypetide-and steroid hormones, neuropeptides, neurotransmitters and neurotrophins, the (neuro-) endocrine controls of hair follicle epithelial stem cell (HFeSC) biology remain to be systematically explored.Focussing on HFeSCs, we attempt here to offer a "roadmap through terra incognita" by listing key open questions, by exploring endocrinologically relevant HFeSC gene profiling and mouse genomics data, and by sketching several clinically relevant pathways via which systemic and/or locally generated (neuro-)endocrine signals might impact on HFeSC. Exemplarily, we discuss e.g. the potential roles of glucocorticoid and vitamin D receptors, the hairless gene product, thymic hormones, bone morphogenic proteins (BMPs) and their antagonists, and Skg-3 in HFeSC biology. Furthermore, we elaborate on the potential role of nerve growth factor (NGF) and substance P-dependent neurogenic inflammation in HFeSC damage, and explore how neuroendocrine signals may influence the balance between maintenance and destruction of hair follicle immune privilege, which protects these stem cells and their progeny. These considerations call for a concerted research effort to dissect the (neuro)-endocrinology of HFeSCs much more systematically than before. The hair follicle (HF) and its special, associated mesenchyme (i.e. the connective tissue sheath, CTS) are repositories of different types of somatic stem cells (epithelial, mesenchymal, neural, mesenchymal) (Cotsarelis, 2006; Kruse et al., 2006;Millar, 2005;Ohyama et al., 2006;Tiede et al. 2007;Waters et al., 2007;Yu et al., 2006). These HFassociated stem cell populations are critical for HF development and function, including HF pigmentation (Nishimura et al., 2002(Nishimura et al., , 2005Sarin and Artandi, 2007). Fig. 1 shows several important, recognized hair follicle-associated stem cell populations and their bestcharacterized location(s) in the pilosebaceous unit, though it must be kept in mind that the indicated ones are unlikely to be the only stem cell population associated with mammalian skin appendages (Tiede et al. 2007). Clinical importance of hair follicle stem cellsHair follicle epithelial stem cells (HFeSCs) are clinically important, since they can be key targets for pathological processes, such as an autoaggressive inflammatory cell attack on HFeSC, e.g. in lupus erythematosus or lichen planopilaris, where the destruction of bulge HFeSCs (see Fig.1) abolishes the hair follicle's capacity to cycle and to rhythmically regenerate itself, leading to scarring alopecia (Cotsarelis, 2006;Hiroi et al., 2006;Mobini et al., 2005;Paus, 2006). Likewise, a gradual loss of HF melanocyte stem cells may exhaust the HF pigmentary unit's capacity to generate itself and to produce melanin and thus likely plays a key role in hair graying (Commo et al., 2004;...

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Section: Clinical Importance Of Hair Follicle Stem Cellsmentioning

confidence: 99%

Section: Pointers From Hfesc Gene Profiling Studiesmentioning

confidence: 99%

Section: Neuroendocrine Controls Of Hair Follicle Immune Privilege Anmentioning

confidence: 99%

mentioning

confidence: 99%

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(Neuro-)endocrinology of epithelial hair follicle stem cells

Paus

Arck

Tiede

2008

Molecular and Cellular Endocrinology

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“…This relative immune privilege is established mainly by suppression of the surface molecules required for presenting autoantigens to CD8+ T lymphocytes and by the generation of an overall immunoinhibitory local signaling milieu. [10][11][12] Some people are genetically predisposed to abnormalities in the microenvironment of the follicle, allowing follicular autoantigens to be presented to preexisting autoreactive CD8+ T cells. When various costimulatory circumstances occur during anagen (e.g., trauma, infection, stress), the clinical phenotype of AA results.…”

Section: Theory Of Immune Privilegementioning

confidence: 99%

Alopecia Areata: An Update

Jerajani¹,

Rohatgi²,

Agrawal³

2017

MGM Journal of Medical Sciences

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Alopecia areata (AA) is a very common autoimmune disease that leads to unpredictable, relapsing patchy hair loss. Its chronic pathophysiology is still not fully understood. Hair follicles are not destroyed permanently due to which the potential for regrowth of hair is retained for many years, and is possibly lifelong. Clinical presentation varies from small alopecia patches most commonly on the scalp to full body involvement. Characteristic "swarm of bees" appearance on histopathology is confirmatory in acute cases. A variety of therapeutic options are available, but search for new modalities continues as there is a high relapse rate and a number of side effects associated with the available treatment options.

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Skin: Immunological Defence Mechanisms

Nickoloff

2007

Encyclopedia of Life Sciences

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Human skin is the largest organ of the body providing a protective coat to ensure that exogenous ‘noxious’ agents do not jeopardize the function of vital internal organ systems. Being situated at the interface between external and internal milieus, a number of remarkable structural and functional characteristics of skin have been delineated that contribute to its effectiveness at maintaining homeostasis.

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A ?hairy? privilege

Cited by 292 publications

References 61 publications

(Neuro-)endocrinology of epithelial hair follicle stem cells

(Neuro-)endocrinology of epithelial hair follicle stem cells

Alopecia Areata: An Update

Skin: Immunological Defence Mechanisms

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