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      Vitamin D and the skin: Focus on a complex relationship: A review

      review-article
      Author(s): * ,
      Publication date (Electronic):
      Journal: Journal of Advanced Research
      Publisher: Elsevier
      Keywords: Vitamin D, Deficiency, Dermatology, Immunological

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          Abstract

          The “sunshine” vitamin is a hot topic that attracted ample attention over the past decades, specially that a considerable proportion of the worldwide population are deficient in this essential nutrient. Vitamin D was primarily acknowledged for its importance in bone formation, however; increasing evidence point to its interference with the proper function of nearly every tissue in our bodies including brain, heart, muscles, immune system and skin. Thereby its deficiency has been incriminated in a long panel of diseases including cancers, autoimmune diseases, cardiovascular and neurological disorders. Its involvement in the pathogenesis of different dermatological diseases is no exception and has been the subject of much research over the recent years. In the current review, we will throw light on this highly disputed vitamin that is creating a significant concern from a dermatological perspective. Furthermore, the consequences of its deficiency on the skin will be in focus.

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          Regulatory T cells and Foxp3.

          Alexander Rudensky (2011)
          Regulatory T (Treg) cells play central role in regulation of immune responses to self-antigens, allergens, and commensal microbiota as well as immune responses to infectious agents and tumors. Transcriptional factor Foxp3 serves as a lineage specification factor of Treg cells. Paucity of Treg cells due to loss-of-function mutations of the Foxp3 gene is responsible for highly aggressive, fatal, systemic immune-mediated inflammatory lesions in mice and humans. Recent studies of Foxp3 expression and function provided critical novel insights into biology of Treg cells and into cellular mechanisms of the immune homeostasis. © 2011 John Wiley & Sons A/S.
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            Cutting edge: 1,25-dihydroxyvitamin D3 is a direct inducer of antimicrobial peptide gene expression.

            Tian-Tian Wang, Frederick Nestel, Véronique Bourdeau … (2004)
            The hormonal form of vitamin D(3), 1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)), is an immune system modulator and induces expression of the TLR coreceptor CD14. 1,25(OH)(2)D(3) signals through the vitamin D receptor, a ligand-stimulated transcription factor that recognizes specific DNA sequences called vitamin D response elements. In this study, we show that 1,25(OH)(2)D(3) is a direct regulator of antimicrobial innate immune responses. The promoters of the human cathelicidin antimicrobial peptide (camp) and defensin beta2 (defB2) genes contain consensus vitamin D response elements that mediate 1,25(OH)(2)D(3)-dependent gene expression. 1,25(OH)(2)D(3) induces antimicrobial peptide gene expression in isolated human keratinocytes, monocytes and neutrophils, and human cell lines, and 1,25(OH)(2)D(3) along with LPS synergistically induce camp expression in neutrophils. Moreover, 1,25(OH)(2)D(3) induces corresponding increases in antimicrobial proteins and secretion of antimicrobial activity against pathogens including Pseudomonas aeruginosa. 1,25(OH)(2)D(3) thus directly regulates antimicrobial peptide gene expression, revealing the potential of its analogues in treatment of opportunistic infections.
            Article 0 comments Cited 246 times – based on 0 reviews     Review now
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              Modulatory effects of 1,25-dihydroxyvitamin D3 on human B cell differentiation.

              Sheng Chen, Gary P. Sims, Xiao Chen … (2007)
              1,25-Dihydroxyvitamin D(3) (1,25(OH)(2)D(3)) can modulate immune responses, but whether it directly affects B cell function is unknown. Patients with systemic lupus erythematosus, especially those with antinuclear Abs and increased disease activity, had decreased 1,25(OH)(2)D(3) levels, suggesting that vitamin D might play a role in regulating autoantibody production. To address this, we examined the effects of 1,25(OH)(2)D(3) on B cell responses and found that it inhibited the ongoing proliferation of activated B cells and induced their apoptosis, whereas initial cell division was unimpeded. The generation of plasma cells and postswitch memory B cells was significantly inhibited by 1,25(OH)(2)D(3), although the up-regulation of genetic programs involved in B cell differentiation was only modestly affected. B cells expressed mRNAs for proteins involved in vitamin D activity, including 1 alpha-hydroxylase, 24-hydroxylase, and the vitamin D receptor, each of which was regulated by 1,25(OH)(2)D(3) and/or activation. Importantly, 1,25(OH)(2)D(3) up-regulated the expression of p27, but not of p18 and p21, which may be important in regulating the proliferation of activated B cells and their subsequent differentiation. These results indicate that 1,25(OH)(2)D(3) may play an important role in the maintenance of B cell homeostasis and that the correction of vitamin D deficiency may be useful in the treatment of B cell-mediated autoimmune disorders.
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                Author and article information

                Contributors
                Wedad Z. Mostafa
                Journal
                Journal ID (nlm-ta): J Adv Res
                Journal ID (iso-abbrev): J Adv Res
                Title: Journal of Advanced Research
                Publisher: Elsevier
                ISSN (Print): 2090-1232
                ISSN (Electronic): 2090-1224
                Publication date PMC-release: 08 February 2014
                Publication date (Print): November 2015
                Publication date (Electronic): 08 February 2014
                Volume: 6
                Issue: 6
                Pages: 793-804
                Affiliations
                Department of Dermatology, Faculty of Medicine, Cairo University, Cairo, Egypt
                Author notes
                [* ]Corresponding author. Tel.: +20 2 33377419, +20 122 2129027. wedad_mostafa@ 123456kasralainy.edu.eg
                Article
                Publisher ID: S2090-1232(14)00023-X
                DOI: 10.1016/j.jare.2014.01.011
                PMC ID: 4642156
                PubMed ID: 26644915
                SO-VID: 1aac1983-4b5f-4d93-bf19-565a7ba19fd4
                Copyright © © 2014 Production and hosting by Elsevier B.V. on behalf of Cairo University.
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/3.0/).

                History
                Date received : 30 November 2013
                Date revision received : 29 January 2014
                Date accepted : 30 January 2014
                Categories
                Subject: Review

                Keywords: vitamin d,deficiency,dermatology,immunological
                Data availability:
                Keywords: vitamin d, deficiency, dermatology, immunological

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