Effect of UVB 311 nm irradiation on normal human skin

被引:22
|
作者
Viac, J
Goujon, C
Misery, L
Staniek, V
Faure, M
Schmitt, D
Claudy, A
机构
[1] Clinique Dermatologique, INSERM U346, Hôpital Ed Hernot, Lyon
[2] INSERM U346, Clinique Dermatologique, Hôpital Ed Herriot
关键词
UVB; normal human skin; Langerhans cells; adhesion molecules; substance P receptors;
D O I
10.1111/j.1600-0781.1997.tb00125.x
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100206 ;
摘要
Ultraviolet radiation B (UVB) on the skin induces erythema, inflammation and modifications of the immune system. These changes have been reported after excessive short-term or long-term exposure to broad spectrum UVB. In this study, we examined the effects of local repetitive UVB irradiation of 311 nm wavelength on the skin of seven young volunteers. Skin biopsies were taken before and after UVB irradiation, and we immunohistochemically analyzed the expression of CD1a and HLA-DR antigens of Langerhans cells (LC), the possible infiltration of dermis/epidermis by CD11b macrophages, the modifications orthe induction of intercellular adhesion molecule-1 (ICAM-1), E-selectin and vascular cell adhesion molecule-1 (VCAM-1) involved in the binding of leukocytes to the endothelial surface and the development of perivascular infiltrates of LFA-1(+) mononuclear cells. We also determined the expression of substance P receptors (SPR) using biotinylated substance P (SPB). Exposure of UVB 311 nm induced a drastic reduction of CD1a(+) cells and a moderate increase of HLA-DR+ dendritic cells in the epidermis without infiltration by CD11b macrophages. An increase of the binding of SPB to upper layer epidermal cells was noted in five of seven biopsies. In the dermis, vessel-associated ICAM-1 expression increased and an induction of E-selectin occurred on nearly 20 to 40% of endothelial cells, but VCAM-1 expression remained undetectable. The percentage of LFA-1(+) cells did not change significantly after irradiation. These observations may be compatible with a selective role of WE 311 nm on the skin immune response.
引用
收藏
页码:103 / 108
页数:6
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