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• W986307265 abstract "Ultraviolet radiation (UVR) causes mutagenic DNA damage to skin cells andsuppression of the skin immune system (SIS) that contributes to skin cancerdevelopment. UVR in the UVB range also causes the beneficial production of vitaminD3 by keratinocytes. Keratinocytes also contain the enzymes required for the two-stephydroxylation of vitamin D3 is to its biologically active form: 1α,25 dihydroxyvitaminD3 (1α,25 (OH)2D3). 1α,25 (OH)2D3 has been demonstrated to modulate the SIS andits response to UVB irradiation. Topical application of 1α,25 (OH)2D3 suppresses theSIS and protects against UV-induced DNA damage. This thesis investigates thehypothesis that dietary vitamin D3 similarly suppresses the SIS response via modulationof the SIS and protects against UVB induced immunosuppression via a reduction inUVB induced DNA damage.To assess the influence of vitamin D3 on the development and function of the SIS, andthe skins response to UVR, a vitamin D3 deficient mouse population was developed.Breeding pairs of vitamin D3 replete and vitamin D3 deficient mice were formed andthe off-spring of these mice were used in experiments. The contact hypersensitivity(CHS) response was used to assess the SIS function in vitamin D3 replete and vitaminD3 deficient mice. In this model the application of the contact sensitiser to the skin ofneonatal mice leads to suppression of the CHS response upon subsequent resensitisationand elicitation of the CHS in adulthood. The suppression of the CHSresponse is termed ‘neonatal tolerance’.Vitamin D3 enhanced neonatal tolerance in male but not female mice. The enhancedneonatal tolerance induction related to an increase in the proportion of CD4+CD25+cells in vitamin D3 replete neonatal male mice and this cell population could transfertolerance in this mouse group. Vitamin D3 suppressed the CHS response in adult malebut not adult female mice. An investigation of DC function in adult mice revealed nomodulation by vitamin D3 in antigen carriage or co-stimulatory molecule expression,suggesting that these cells were not modulating the reduced CHS response in adult malemice. However, dietary vitamin D3 was associated with a higher proportion of CD4+CD25+ cells in the SDLN after contact sensitiser application in male but notfemale mice, implying that vitamin D3 was modulating the induction of these cells.The level of UVB-induced immunosuppression was assessed in vitamin D3 replete anddeficient mice in C57BL/6 and BALB/c mice. Vitamin D3 protected C57BL/6, but notBALB/c mice against UVB-induced immunosuppression. The protection against UVBinducedimmunosuppression may relate to a reduction in UVB-induced DNA damage inC57BL/6 mice, not identified in BALB/c mice. In BALB/c mice female genderprotected against UVB-induced immunosuppression and was associated with a subtlelowering of UVB-induced DNA damage in comparison to male mice at low UVRexposures. These results indicate that the protection against UVB-inducedimmunosuppression by vitamin D3 varies with genetic background and the modulationof UVB-induced DNA damage.If these mouse studies are extended to humans, the ability of vitamin D3 to suppress theSIS and the limited protection against UVB-induced DNA damage in males, dependingon their genetic background, may contribute to the greater burden of skin cancer inmales than in females." @default.
• W986307265 created "2016-06-24" @default.
• W986307265 creator A5001681483 @default.
• W986307265 date "2010-06-01" @default.
• W986307265 modified "2023-09-23" @default.
• W986307265 title "Dietary Vitamin D3, the skin immune system andimplications for skin cancer" @default.
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• W986307265 hasPublicationYear "2010" @default.
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