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Review

Fundamental questions to sun protection

A continuous education symposium at the University of Zürich on "Vitamin D, immune system and sun protection"

Pages 19-25 | Published online: 01 Jan 2010
 

Abstract

Since exposure to sunlight is a main factor in the development of non-melanoma skin cancer and there are associations between malignant melanoma and short-term intense ultraviolet (UV) exposure, particularly burning in childhood, strict protection from UV-radiation is recommended. However, up to 90% of all requisite vitamin-D has to be formed within the skin through the action of the sun - a serious problem, for a connection between vitamin-D deficiency, demonstrated in epidemiological studies, and various types of cancer and other diseases has been confirmed. A UVB-triggered skin autonomous vitamin D3 synthesis pathway has recently been described, producing the active Vitamin D metabolite calcitriol. This cutaneous vitamin D3 pathway is unique. Keratinocytes and dendritic cells can convert vitamin D to calcitriol. Cutaneous T cells activated in the presence of calcitriol express the chemokine receptor CCR10 attracting them to the chemokine CCL27 that keratinocytes express selectively in the epidermis, and migrate from dermal layers of the skin to the epidermis under UV radiation. Thus, calcitriol has endocrine roles beyond its calciotropic action, including cell growth and cancer prevention. Therefore, strict sun protection procedures to prevent skin cancer may induce the risk of vitamin-D deficiency. As there is evidence that the protective effect of less intense solar radiation can outweigh its mutagenic effect, better balanced approaches to sun protection should be sought.

Figures and Tables

Figure 1 UVB rays from sunlight generates vitamin D3 from its precursor in the skin. Vitamin D3 is not very active and can be converted to both 25(OH)D3 and 1,25(OH)2D3 by dendritic cells. Dendritic cells come in close contact with T cells, and in the presence of vitamin D3, the CCR10 receptor is induced on the T cells. This attracts the T cells to CCL27, which is selectively produced and secreted by keratinocytes in the epidermis. Thus, once T cells have infiltrated the dermal layers of the skin from the cutaneous blood vessel, they can be mobilized within the skin and migrate to the epidermis. This way, T cells could be drawn to the epidermis when they are needed.

Figure 1 UVB rays from sunlight generates vitamin D3 from its precursor in the skin. Vitamin D3 is not very active and can be converted to both 25(OH)D3 and 1,25(OH)2D3 by dendritic cells. Dendritic cells come in close contact with T cells, and in the presence of vitamin D3, the CCR10 receptor is induced on the T cells. This attracts the T cells to CCL27, which is selectively produced and secreted by keratinocytes in the epidermis. Thus, once T cells have infiltrated the dermal layers of the skin from the cutaneous blood vessel, they can be mobilized within the skin and migrate to the epidermis. This way, T cells could be drawn to the epidermis when they are needed.