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Jin, R.; , . The Trinity of Skin: A Neuro–Endocrine–Immune Organ. Encyclopedia. Available online: https://encyclopedia.pub/entry/23406 (accessed on 23 April 2024).
Jin R,  . The Trinity of Skin: A Neuro–Endocrine–Immune Organ. Encyclopedia. Available at: https://encyclopedia.pub/entry/23406. Accessed April 23, 2024.
Jin, Rong, . "The Trinity of Skin: A Neuro–Endocrine–Immune Organ" Encyclopedia, https://encyclopedia.pub/entry/23406 (accessed April 23, 2024).
Jin, R., & , . (2022, May 26). The Trinity of Skin: A Neuro–Endocrine–Immune Organ. In Encyclopedia. https://encyclopedia.pub/entry/23406
Jin, Rong and . "The Trinity of Skin: A Neuro–Endocrine–Immune Organ." Encyclopedia. Web. 26 May, 2022.
The Trinity of Skin: A Neuro–Endocrine–Immune Organ
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This entry is adapted from the peer-reviewed paper 10.3390/life12050725

For a long time, skin was thought to be no more than the barrier of human's body. However, in the last few decades, studies into the idea of skin as an independent functional organ have gradually deepened people's understanding of skin and its functions.

skin neuro–endocrine–immune

1. Introduction

The skin is the largest organ of the human body, protecting internal homeostasis from the external environment. However, skin is not only a simple barrier, but also involved in maintaining internal homeostasis through bidirectional communications between the central nervous, endocrine and immune systems. As far back as 1998, the idea of a neuro–immune–cutaneous–endocrine network was developed and initialized as “NICE” [1], although the endocrine aspect was not elucidated in these early articles. Shifting the focus to the present day, emerging evidence has gradually verified that the skin shares and provides the same bioactive molecules as the body, especially the evidence of cutaneous production and action of neuropeptides, hormones and cytokines. This suggests the existence of cross-talk between the skin and the system, and gives the skin a new identity of a neuro–endocrine–immune organ.

2. Neuro Function of Skin

The term “neurogenic inflammation” suggests the critical role of the cutaneous nervous system in immune response and homeostasis. Chronic inflammatory skin diseases such as atopic dermatitis (AD) and psoriasis can be aggravated by stress [2][3][4][5][6], which is a good example of neurogenic inflammation.

2.1. Anatomic Foundation of Cutaneous Nervous System

Skin is derived from ectoderm, like the nervous system, which makes it easier to understand the diverse nervous function of skin. Skin is innervated with mostly sensory nerves, classified into A-β, A-δ and C fibers according to their diameter, myelinization, and velocity of conduction [7]. A-β fibers are highly myelinated, rapid conducting fibers and innervating specialized mechanosensory end organs that include Meissner’s corpuscles, Pacinian corpuscles, Merkel cells, and Ruffini corpuscles [8][9]. A-δ fibers are less myelinated fibers with slower conduction velocity that give sensation to mechanical, heat nociception and non-noxious cold thermal stimuli. C fibers are unmyelinated fibers with the lowest conducting speed, precept thermal and chemical and mechanical stimuli [10][11][12]. Along these fibers lies immune cells such as mast cells [13][14], dendritic cells [15][16], macrophages [17], innate lymphoid cells [18] and γδT cells [19], forming neuroimmune cell units (NICUs) that orchestrate skin homeostasis [20][21].

2.2. Neuroimmune Interactions of Skin

The cutaneous nervous system and immune system have a responsibility in common: sensing. Whether recognizing pathogens through immune cells or precepting noxious stimuli via sensory nerves, these two “sensing” systems of the skin work synergistically against environmental challenges.
Upon sensing stimuli, especially noxious ones, the cutaneous nervous system tends to communicate with the immune system via neurotrophins (NTs) and neuropeptides (NPs), causing subsequent cascading effects known as “neuroimmune interactions” [22][23][24][25]. NTs belong to a family of growth factors that control the development, maintenance, and apoptosis of neurons and regulate skin homeostasis; for example, the stimulation of mast cell degranulation and cytokine release [26]. NPs, such as substance P (SP), calcitonin gene-related protein (CGRP) and hundreds of other types, are secreted by cutaneous nerves [27]. SP induces mast cell degranulation and the release of histamine and vascular endothelial growth factor (VEGF), subsequently causing proinflammatory effects, hypervascularization and infiltration of inflammatory cells [28][29]. CGRP is involved in vasodilation and neurogenic inflammation [30].
However, neuroimmune reaction of the skin is bidirectional. The cutaneous nervous system also takes orders from the immune system through cytokines. Immune cells sense pathogenic events though a set of receptors, recognizing pathogen-associated molecular patterns (PAMPs) such as LPS and CpG, and damage-associated molecular patterns (DAMPs); for instance, HMGB1, S100 proteins and heat-shock proteins [31][32][33]. Such pattern-recognition receptors (PRRs) such as Toll-like receptors (TLRs) and IL-1R, after binding with PAMPs and DAMPs, lead to inflammatory and immune responses through signaling to nuclear factor kB (NF-kB) [34], inducing the expression of proinflammatory cytokines such as IL-1, -6, -31, IFN-I and TNF-α [35][36]. With cytokine serving as ligands and activators of sensory nerves [37], downstream neuro effects take place. For example, IL-6 induces the expression of nerve growth factor (NGF) and NT-3, 4, and 5 [38][39], while IL-31 exerts its pruritic effects [40].

2.3. Skin-CNS Connection

The cutaneous nervous system, as part of the peripheral nervous system, sends and receives messages from the central nervous system (CNS), which can be elucidated using the model of pruritus. Itch receptors on neuropeptide-containing free nerve endings can be directly set off by histamine and other pruritogens, or indirectly by cytokine-induced histamine release [41]. Once an action potential is set off, it travels through the dorsal root ganglia onto the spinal cord, eventually to the somatosensory cortex in the brain. Conversely, CNS also participate in the modulation and inhibition of peripheral pruritis via periaqueductal grey matter (PAG) of the mid-brain [42][43]. Additionally, psychological stress can aggravate pruritus [44][45], which is another solid evidence of skin–CNS connection.

3. Endocrine Function of Skin

3.1. Skin as Endocrine End Organ

Skin is the target of several hormones and expresses a number of endocrine receptors. For example, glucocorticoids (GCs) and mineralocorticoids (MCs) interfere with the epidermal development and homeostasis through GC receptor (GR/NR3C1) and mineralocorticoid receptor (MR/NR3C2), both of which are members of the nuclear receptor (NR) subclass NR3C and are present in all skin compartments [46]. Like GCs and MCs, thyroid hormones (THs) also participate in epidermal development and homeostasis via nuclear thyroid hormone receptors (TRs) TRα and TRβ, expressed in epidermal and dermal cells [47]. Androgen receptors in sebaceous glands and hair follicles regulate sebum secretion and hair growth [48]; insulin receptor and insulin-like growth factor 1 (IGF-1) receptor in keratinocytes (KCs) modify cutaneous development and metabolism [49]. In conclusion, various kinds of hormones bring their biological effects into skin through binding with cutaneous endocrine receptors. Therefore, when the systemic endocrine function is compromised, cutaneous homeostasis will also be influenced. There are abundant supporting clinical findings such as the correlation between acanthosis nigricans, acrochordon and metabolic syndrome in patients with lichen planus [50]; the connection between alopecia areata, vitiligo and autoimmune thyroid disease [51]; and the relationship between acne, hypertrichosis and insulin resistance [52].

3.2. Skin as Endocrine Initiating Organ

Hormones are synthesized in skin mainly through two ways: activation of circulating hormone precursors and de novo synthesis. Examples of the former way include the activation of cortisol and corticosterone through local 11β-hydroxysteroid dehydrogenase (11β-HSD) [53] and the intracellular T4 conversion into T3 via iodothyronine deiodinase enzymes D1 and D2 [47]. Both GCs and THs are essential for skin homeostasis, GCs downregulate inflammation [54] while THs enhance skin susceptibility to inflammation [55]. Another well-known example of hormone activation is the conversion of dehydroepiandrosterone (DHEA) to androstenedione, then to testosterone through isotypes of 17β-hydroxysteroid dehydrogenase (17β-HSD) in skin. Further conversion of testosterone into its most potent form, 5α-dihydrotestosterone (5α-DHT), is completed by 5α-reductase in skin [56].
Other than in traditional endocrine organs, de novo synthesis of hormones also takes place in skin. The most studied example is the equivalent of hypothalamic-pituitary-adrenal (HPA) axis in skin. The traditional adaptive responses to systemic stress are regulated by the HPA axis. Activation of the traditional HPA axis begins with the pituitary production of the corticotropin-releasing hormone (CRH) following stimulation by corticotrophin-releasing factor (CRF) secreted from the hypothalamus. Then, CRH receptor type 1 in the anterior pituitary is activated and induces the cleavage of proopiomelanocortin (POMC) into the adrenocorticotropic hormone (ACTH), α-melanocyte-stimulating hormone (α-MSH) and β-endorphin (β-END) [57]. ACTH stimulates the adrenal cortex to secret GCs, which responds to stressors and suppresses the HPA axis through negative feedback [57].
When stressors come to the skin, KCs produce hormonal products, similar to that produced in systemic stressful events such as CRH, POMC, β-END, ACTH and α-MSH [58]. Moreover, enzymes of corticosteroid synthesis such as CYP11A1, 3β-HSD, CPY17A1, CYP21A2 and CYP11B1 are expressed in KCs and thus produce corticosterone and cortisol [59][60], which further proves the existence of the skin HPA axis. In an IMQ-treated mouse model whose KC-derived CYP11B1 was knocked out, local homeostasis was impaired and psoriasiform inflammation was exacerbated. Furthermore, even non-IMQ-treated mice presented psoriasiform inflammation after CYP11B1 knock out, showing the homeostasis stabilizing effect of KC-derived GC and the importance of the whole skin equivalent of the HPA axis [54].
Apart from the well-known GCs, vitamin D and its analogs are known as secosteroids, which is synthesized from the skin. In KCs of the basal layer of epidermis, 7-dehydrocholesterol (7-DHC) is converted to vitamin D3 under UVB light, then released into system to further undergo biological activation in the hepatocytes and kidneys [61]. Numerous skin functions are regulated by vitamin D and its receptor, including coregulation in epidermal proliferation and differentiation [62], regulation of the hair follicle cycle [63], promotion of innate immunity [64], and suppression of tumor formation and inflammation [65]. Vitamin D disturbance is often seen in skin diseases, such as low vitamin D status in psoriasis [66] and chronic urticaria patients [67], and elevated vitamin D level in rosacea patients [68].

References

  1. O’Sullivan, R.L.; Lipper, G.; Lerner, E.A. The neuro-immuno-cutaneous-endocrine network: Relationship of mind and skin. Arch. Dermatol. 1998, 134, 1431–1435.
  2. Lin, T.K.; Zhong, L.; Santiago, J.L. Association between Stress and the HPA Axis in the Atopic Dermatitis. Int. J. Mol. Sci. 2017, 18, 2131.
  3. Mochizuki, H.; Lavery, M.J.; Nattkemper, L.A.; Albornoz, C.; Valdes Rodriguez, R.; Stull, C.; Weaver, L.; Hamsher, J.; Sanders, K.M.; Chan, Y.H.; et al. Impact of acute stress on itch sensation and scratching behaviour in patients with atopic dermatitis and healthy controls. Br. J. Dermatol. 2019, 180, 821–827.
  4. Yang, H.; Li, X.; Zhang, L.; Xue, F.; Zheng, J. Immunomodulatory effects of sleep deprivation at different timing of psoriasiform process on skin inflammation. Biochem. Biophys. Res. Commun. 2019, 513, 452–459.
  5. Yang, H.; Zheng, J. Influence of stress on the development of psoriasis. Clin. Exp. Dermatol. 2020, 45, 284–288.
  6. Bozo, R.; Danis, J.; Flink, L.B.; Vidacs, D.L.; Kemeny, L.; Bata-Csorgo, Z. Stress-Related Regulation Is Abnormal in the Psoriatic Uninvolved Skin. Life 2021, 11, 599.
  7. Glatte, P.; Buchmann, S.J.; Hijazi, M.M.; Illigens, B.M.; Siepmann, T. Architecture of the Cutaneous Autonomic Nervous System. Front. Neurol. 2019, 10, 970.
  8. Fleming, M.S.; Luo, W. The anatomy, function, and development of mammalian Abeta low-threshold mechanoreceptors. Front. Biol. 2013, 8, 408–420.
  9. Cobo, R.; Garcia-Piqueras, J.; Cobo, J.; Vega, J.A. The Human Cutaneous Sensory Corpuscles: An Update. J. Clin. Med. 2021, 10, 227.
  10. Lawson, S.N. Phenotype and Function of Somatic Primary Afferent Nociceptive Neurones with C-, Adelta- or Aalpha/beta-Fibres. Exp. Physiol. 2002, 87, 239–244.
  11. Djouhri, L. Adelta-fiber low threshold mechanoreceptors innervating mammalian hairy skin: A review of their receptive, electrophysiological and cytochemical properties in relation to Adelta-fiber high threshold mechanoreceptors. Neurosci. Biobehav. Rev. 2016, 61, 225–238.
  12. Schmelz, M.; Schmidt, R.; Weidner, C.; Hilliges, M.; Torebjork, H.E.; Handwerker, H.O. Chemical response pattern of different classes of C-nociceptors to pruritogens and algogens. J. Neurophysiol. 2003, 89, 2441–2448.
  13. Gupta, K.; Harvima, I.T. Mast cell-neural interactions contribute to pain and itch. Immunol. Rev. 2018, 282, 168–187.
  14. Meixiong, J.; Basso, L.; Dong, X.; Gaudenzio, N. Nociceptor-Mast Cell Sensory Clusters as Regulators of Skin Homeostasis. Trends Neurosci. 2020, 43, 130–132.
  15. Veiga-Fernandes, H.; Mucida, D. Neuro-Immune Interactions at Barrier Surfaces. Cell 2016, 165, 801–811.
  16. Kabashima, K.; Honda, T.; Ginhoux, F.; Egawa, G. The immunological anatomy of the skin. Nat. Rev. Immunol. 2019, 19, 19–30.
  17. Kolter, J.; Feuerstein, R.; Zeis, P.; Hagemeyer, N.; Paterson, N.; d’Errico, P.; Baasch, S.; Amann, L.; Masuda, T.; Losslein, A.; et al. A Subset of Skin Macrophages Contributes to the Surveillance and Regeneration of Local Nerves. Immunity 2019, 50, 1482–1497.e7.
  18. Kobayashi, T.; Ricardo-Gonzalez, R.R.; Moro, K. Skin-Resident Innate Lymphoid Cells—Cutaneous Innate Guardians and Regulators. Trends Immunol. 2020, 41, 100–112.
  19. Marshall, A.S.; Silva, J.R.; Bannerman, C.A.; Gilron, I.; Ghasemlou, N. Skin-Resident gammadelta T Cells Exhibit Site-Specific Morphology and Activation States. J. Immunol. Res. 2019, 2019, 9020234.
  20. Veiga-Fernandes, H.; Artis, D. Neuronal-immune system cross-talk in homeostasis. Science 2018, 359, 1465–1466.
  21. Blake, K.J.; Jiang, X.R.; Chiu, I.M. Neuronal Regulation of Immunity in the Skin and Lungs. Trends Neurosci. 2019, 42, 537–551.
  22. Ordovas-Montanes, J.; Rakoff-Nahoum, S.; Huang, S.; Riol-Blanco, L.; Barreiro, O.; von Andrian, U.H. The Regulation of Immunological Processes by Peripheral Neurons in Homeostasis and Disease. Trends Immunol. 2015, 36, 578–604.
  23. Choi, J.E.; Di Nardo, A. Skin neurogenic inflammation. In Seminars in Immunopathology; Springer: Berlin/Heidelberg, Germany, 2018; pp. 249–259.
  24. Vidal Yucha, S.E.; Tamamoto, K.A.; Kaplan, D.L. The importance of the neuro-immuno-cutaneous system on human skin equivalent design. Cell Prolif. 2019, 52, e12677.
  25. Dantzer, R. Neuroimmune interactions: From the brain to the immune system and vice versa. Physiol. Rev. 2018, 98, 477–504.
  26. Botchkarev, V.A.; Yaar, M.; Peters, E.M.; Raychaudhuri, S.P.; Botchkareva, N.V.; Marconi, A.; Raychaudhuri, S.K.; Paus, R.; Pincelli, C. Neurotrophins in skin biology and pathology. J. Investig. Dermatol. 2006, 126, 1719–1727.
  27. Russo, A.F. Overview of Neuropeptides: Awakening the Senses? Headache 2017, 57 (Suppl. S2), 37–46.
  28. Li, W.W.; Guo, T.Z.; Liang, D.Y.; Sun, Y.; Kingery, W.S.; Clark, J.D. Substance P signaling controls mast cell activation, degranulation, and nociceptive sensitization in a rat fracture model of complex regional pain syndrome. Anesthesiology 2012, 116, 882–895.
  29. Theoharides, T.C. The impact of psychological stress on mast cells. Ann. Allergy Asthma Immunol. 2020, 125, 388–392.
  30. Schlereth, T.; Schukraft, J.; Kramer-Best, H.H.; Geber, C.; Ackermann, T.; Birklein, F. Interaction of calcitonin gene related peptide (CGRP) and substance P (SP) in human skin. Neuropeptides 2016, 59, 57–62.
  31. Bianchi, M.E. DAMPs, PAMPs and alarmins: All we need to know about danger. J. Leukoc. Biol. 2007, 81, 1–5.
  32. Zindel, J.; Kubes, P. DAMPs, PAMPs, and LAMPs in Immunity and Sterile Inflammation. Annu. Rev. Pathol. 2020, 15, 493–518.
  33. Gong, T.; Liu, L.; Jiang, W.; Zhou, R. DAMP-sensing receptors in sterile inflammation and inflammatory diseases. Nat. Rev. Immunol. 2020, 20, 95–112.
  34. Verstrepen, L.; Bekaert, T.; Chau, T.L.; Tavernier, J.; Chariot, A.; Beyaert, R. TLR-4, IL-1R and TNF-R signaling to NF-kappaB: Variations on a common theme. Cell Mol. Life Sci. 2008, 65, 2964–2978.
  35. Yu, H.; Lin, L.; Zhang, Z.; Zhang, H.; Hu, H. Targeting NF-kappaB pathway for the therapy of diseases: Mechanism and clinical study. Signal Transduct. Target. Ther. 2020, 5, 209.
  36. Maier, E.; Werner, D.; Duschl, A.; Bohle, B.; Horejs-Hoeck, J. Human Th2 but not Th9 cells release IL-31 in a STAT6/NF-kappaB-dependent way. J. Immunol. 2014, 193, 645–654.
  37. Roosterman, D.; Goerge, T.; Schneider, S.W.; Bunnett, N.W.; Steinhoff, M. Neuronal control of skin function: The skin as a neuroimmunoendocrine organ. Physiol. Rev. 2006, 86, 1309–1379.
  38. Minnone, G.; De Benedetti, F.; Bracci-Laudiero, L. NGF and Its Receptors in the Regulation of Inflammatory Response. Int. J. Mol. Sci. 2017, 18, 1028.
  39. Marz, P.; Heese, K.; Dimitriades-Schmutz, B.; Rose-John, S.; Otten, U. Role of interleukin-6 and soluble IL-6 receptor in region-specific induction of astrocytic differentiation and neurotrophin expression. Glia 1999, 26, 191–200.
  40. Furue, M.; Yamamura, K.; Kido-Nakahara, M.; Nakahara, T.; Fukui, Y. Emerging role of interleukin-31 and interleukin-31 receptor in pruritus in atopic dermatitis. Allergy 2018, 73, 29–36.
  41. Stander, S.; Steinhoff, M. Pathophysiology of pruritus in atopic dermatitis: An overview. Exp. Dermatol. 2002, 11, 12–24.
  42. Mochizuki, H.; Tashiro, M.; Kano, M.; Sakurada, Y.; Itoh, M.; Yanai, K. Imaging of central itch modulation in the human brain using positron emission tomography. Pain 2003, 105, 339–346.
  43. Najafi, P.; Dufor, O.; Ben Salem, D.; Misery, L.; Carre, J.L. Itch processing in the brain. J. Eur. Acad. Dermatol. Venereol. 2021, 35, 1058–1066.
  44. Golpanian, R.S.; Kim, H.S.; Yosipovitch, G. Effects of Stress on Itch. Clin. Ther. 2020, 42, 745–756.
  45. Kim, H.J.; Park, J.B.; Lee, J.H.; Kim, I.H. How stress triggers itch: A preliminary study of the mechanism of stress-induced pruritus using fMRI. Int. J. Dermatol. 2016, 55, 434–442.
  46. Sevilla, L.M.; Perez, P. Roles of the Glucocorticoid and Mineralocorticoid Receptors in Skin Pathophysiology. Int. J. Mol. Sci. 2018, 19, 1906.
  47. Mancino, G.; Miro, C.; Di Cicco, E.; Dentice, M. Thyroid hormone action in epidermal development and homeostasis and its implications in the pathophysiology of the skin. J. Endocrinol. Investig. 2021, 44, 1571–1579.
  48. Zouboulis, C.C.; Picardo, M.; Ju, Q.; Kurokawa, I.; Torocsik, D.; Biro, T.; Schneider, M.R. Beyond acne: Current aspects of sebaceous gland biology and function. Rev. Endocr. Metab. Disord. 2016, 17, 319–334.
  49. Wertheimer, E.; Trebicz, M.; Eldar, T.; Gartsbein, M.; Nofeh-Moses, S.; Tennenbaum, T. Differential roles of insulin receptor and insulin-like growth factor-1 receptor in differentiation of murine skin keratinocytes. J. Investig. Dermatol. 2000, 115, 24–29.
  50. Daye, M.; Temiz, S.A.; Isik, B.; Durduran, Y. Relationship between acanthosis nigricans, acrochordon and metabolic syndrome in patients with lichen planus. Int. J. Clin. Pract. 2021, 75, e14687.
  51. Saylam Kurtipek, G.; Cihan, F.G.; Erayman Demirbas, S.; Ataseven, A. The Frequency of Autoimmune Thyroid Disease in Alopecia Areata and Vitiligo Patients. Biomed. Res. Int. 2015, 2015, 435947.
  52. Kubba, R. Insulin Resistance Associated Acne. In Acne: Current Concepts and Management; Suh, D.H., Ed.; Springer International Publishing: Cham, Switzerland, 2021; pp. 95–110.
  53. Terao, M.; Katayama, I. Local cortisol/corticosterone activation in skin physiology and pathology. J. Dermatol. Sci. 2016, 84, 11–16.
  54. Phan, T.S.; Schink, L.; Mann, J.; Merk, V.M.; Zwicky, P.; Mundt, S.; Simon, D.; Kulms, D.; Abraham, S.; Legler, D.F.; et al. Keratinocytes control skin immune homeostasis through de novo-synthesized glucocorticoids. Sci. Adv. 2021, 7, eabe0337.
  55. Mancino, G.; Sibilio, A.; Luongo, C.; Di Cicco, E.; Miro, C.; Cicatiello, A.G.; Nappi, A.; Sagliocchi, S.; Ambrosio, R.; De Stefano, M.A.; et al. The Thyroid Hormone Inactivator Enzyme, Type 3 Deiodinase, Is Essential for Coordination of Keratinocyte Growth and Differentiation. Thyroid 2020, 30, 1066–1078.
  56. Ceruti, J.M.; Leiros, G.J.; Balana, M.E. Androgens and androgen receptor action in skin and hair follicles. Mol. Cell Endocrinol. 2018, 465, 122–133.
  57. Spencer, R.L.; Deak, T. A users guide to HPA axis research. Physiol. Behav. 2017, 178, 43–65.
  58. Slominski, A.; Wortsman, J.; Luger, T.; Paus, R.; Solomon, S. Corticotropin releasing hormone and proopiomelanocortin involvement in the cutaneous response to stress. Physiol. Rev. 2000, 80, 979–1020.
  59. Slominski, A.T.; Manna, P.R.; Tuckey, R.C. Cutaneous glucocorticosteroidogenesis: Securing local homeostasis and the skin integrity. Exp. Dermatol. 2014, 23, 369–374.
  60. Hannen, R.F.; Michael, A.E.; Jaulim, A.; Bhogal, R.; Burrin, J.M.; Philpott, M.P. Steroid synthesis by primary human keratinocytes; implications for skin disease. Biochem. Biophys. Res. Commun. 2011, 404, 62–67.
  61. Bikle, D.D. Vitamin D and the skin: Physiology and pathophysiology. Rev. Endocr. Metab. Disord. 2012, 13, 3–19.
  62. Samuel, S.; Sitrin, M.D. Vitamin D’s role in cell proliferation and differentiation. Nutr. Rev. 2008, 66, S116–S124.
  63. Demay, M.B. The hair cycle and Vitamin D receptor. Arch. Biochem. Biophys. 2012, 523, 19–21.
  64. Schauber, J.; Dorschner, R.A.; Coda, A.B.; Büchau, A.S.; Liu, P.T.; Kiken, D.; Helfrich, Y.R.; Kang, S.; Elalieh, H.Z.; Steinmeyer, A. Injury enhances TLR2 function and antimicrobial peptide expression through a vitamin D–dependent mechanism. J. Clin. Investig. 2007, 117, 803–811.
  65. Krishnan, A.V.; Feldman, D. Mechanisms of the anti-cancer and anti-inflammatory actions of vitamin D. Annu. Rev. Pharmacol. Toxicol. 2011, 51, 311–336.
  66. Barrea, L.; Savanelli, M.C.; Di Somma, C.; Napolitano, M.; Megna, M.; Colao, A.; Savastano, S. Vitamin D and its role in psoriasis: An overview of the dermatologist and nutritionist. Rev. Endocr. Metab. Disord. 2017, 18, 195–205.
  67. Kader, S.; Temiz, S.A.; Akdag, T.; Unlu, A. Evaluation of vitamin D and calcium mineral metabolism in patients with chronic urticaria. Int. J. Med. Biochem. 2021, 4, 157–160.
  68. Ekiz, Ö.; Balta, I.; Şen, B.B.; Dikilitaş, M.C.; Özuğuz, P.; Rifaioğlu, E.N. Vitamin D status in patients with rosacea. Cutan. Ocul. Toxicol. 2014, 33, 60–62.
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