Reeve V E, Domanski D
Faculty of Veterinary Science, McMaster Building B14, University of Sydney, NSW 2006, Australia.
Br J Dermatol. 2003 Jun;148(6):1189-93. doi: 10.1046/j.1365-2133.2003.05345.x.
A protective role for the ultraviolet (UV) A waveband against immunosuppression induced by UVB (280-320 nm) radiation has been identified. The mechanism for UVA immunoprotection was found to involve two apparently unrelated mediators, the T-helper-1-associated proinflammatory cytokine interferon (IFN)-gamma and the UVA-induced redox-regulated stress protein, haem oxygenase (HO).
To identify a relationship between these two immune regulators.
The HO response to UVA radiation in the skin and liver was examined in mice with a targeted disruption of the IFN-gamma gene, known to be unresponsive to UVA photoimmunoprotection. Results IFN-gamma null mice did not respond to UVA irradiation with the normal upregulation of HO activity in either the irradiated skin or the liver. Injection of these mice with recombinant IFN-gamma previously shown to restore the UVA-photoimmunoprotective effect, here partially and dose-responsively restored their ability for induction of HO activity in both skin and liver following UVA irradiation.
IFN-gamma appears to be a prerequisite for the immunoprotective induction of HO, although other mediators may also be involved. The UVA responsiveness of HO in an internal organ such as the liver suggests the existence of a soluble UVA-induced mediator from the skin, which may be IFN-gamma.
已确定紫外线（UV）A波段对UVB（280 - 320纳米）辐射诱导的免疫抑制具有保护作用。发现UVA免疫保护机制涉及两种明显不相关的介质，即辅助性T细胞1相关的促炎细胞因子干扰素（IFN）-γ和UVA诱导的氧化还原调节应激蛋白血红素加氧酶（HO）。
确定这两种免疫调节因子之间的关系。
在已知对UVA光免疫保护无反应的IFN-γ基因靶向破坏的小鼠中，检测皮肤和肝脏对UVA辐射的HO反应。结果IFN-γ基因敲除小鼠在照射的皮肤或肝脏中，对UVA照射未出现正常的HO活性上调反应。给这些小鼠注射先前已证明能恢复UVA光免疫保护作用的重组IFN-γ，在此部分且呈剂量反应性地恢复了它们在UVA照射后皮肤和肝脏中诱导HO活性的能力。
IFN-γ似乎是HO免疫保护诱导的先决条件，尽管可能还涉及其他介质。HO在肝脏等内部器官中对UVA的反应性表明存在一种来自皮肤的可溶性UVA诱导介质，可能是IFN-γ。
