Reeve V E, Ley R D
Department of Veterinary Pathology, University of Sydney, Australia.
Int Arch Allergy Immunol. 1997 Mar;112(3):257-61. doi: 10.1159/000237463.
The suppression of contact hypersensitivity by UVB (280-320 nm) radiation can be prevented by photoreactivating light (PRL; 320-400 nm) in the opossum Monodelphis domestica, implicating epidermal DNA lesions as the immunosuppressive impairment. However, contact hypersensitivity can also be suppressed in the opossum with exogenous cis-urocanic acid, a molecule which is produced in UVB-irradiated epidermis and is a second potential mediator of photo-immunosuppression apparently independent of UVB-induced DNA damage. Here we demonstrate that irradiation of opossums with PRL either before or following treatment with exogenous cis-urocanic acid, significantly reduced the degree of immunosuppression. This suggests that, in addition to its capacity to initiate post-UVB-exposure epidermal DNA repair, the PRL waveband can induce an immunoprotective product, as yet unidentified, in opossum epidermis.
在家负鼠中，紫外线B（UVB，280 - 320纳米）辐射对接触性超敏反应的抑制作用可被光复活光（PRL，320 - 400纳米）逆转，这表明表皮DNA损伤是免疫抑制的原因。然而，外源性顺式尿刊酸也能在家负鼠中抑制接触性超敏反应，顺式尿刊酸是UVB照射表皮产生的一种分子，是光免疫抑制的另一种潜在介质，显然独立于UVB诱导的DNA损伤。在此我们证明，在用外源性顺式尿刊酸处理之前或之后，用PRL照射负鼠，可显著降低免疫抑制程度。这表明，除了启动UVB照射后表皮DNA修复的能力外，PRL波段还能在家负鼠表皮中诱导一种尚未明确的免疫保护产物。
