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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Heme oxygenase induction mediates the photoimmunoprotective activity of UVA radiation in the mouse
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Heme oxygenase induction mediates the photoimmunoprotective activity of UVA radiation in the mouse

机译：血红素加氧酶诱导介导小鼠中UVA辐射的光免疫保护活性

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In contrast to the immunosuppressive potential of UVB (280-320 nM) radiation in experimental animals and humans, UVA (320-400 nm) radiation at environmentally relevant doses appears to be immunologically inert. However, such exposure to UVA radiation has been observed unexpectedly to induce resistance to UVB-induced immunosuppression in mice, by a mechanism resulting in the inactivation of cis.urocanic acid (UCA), an epidermal immunosuppressive UV photoproduct. In this study in mice, we show that the immunoprotective activity of UVA radiation, against the effects of both UTB radiation and cis-UCA, can bc attributed to the induction of cutaneous heme oxygenase (HO; EC l.14.99.3). Cell-mediated immune function was assessed in vivo by the contact hypersensitivity response induced to oxazolone at an unirradiated skin site, and HO enzyme activity was measured in cutaneous microsomal preparations from treated mice. There was a progressive increase in HO enzyme activity for at least 3 days after UVA irradiation. However HO activity, both constitutive and UVA radiation-induced, was sensitive to the effects of injecting mice with the specific HO inhibitor, tin protoporphyrin (Sn [IV'] protoporphyrin IX; SnPP). We observed, in addition, that in SnPP-injected mice, the immunoprotective effect of UVA radiation against either UVB radiation or cis-UCA was abrogated. Because SnPP injection did not affect normal contact hypersensitivity responsiveness but did inhibit the constitutive HO enzyme activity, it appeared that only the inducible HO was active in modulating immune function. This f
机译：与实验动物和人类中UVB（280-320 nM）辐射的免疫抑制潜力相反，与环境有关剂量的UVA（320-400 nm）辐射在免疫学上似乎是惰性的。然而，通过导致表皮免疫抑制性紫外线光产物顺式尿烷酸（UCA）失活的机制，意外地观察到这种暴露于UVA辐射的小鼠诱导出对UVB诱导的免疫抑制的抗性。在小鼠的这项研究中，我们显示UVA辐射针对UTB辐射和顺式UCA的免疫保护活性可归因于皮肤血红素加氧酶的诱导（HO； EC l.14.99.3）。通过在未辐照的皮肤部位诱导对恶唑酮的接触超敏反应，在体内评估了细胞介导的免疫功能，并在来自经治疗的小鼠的皮肤微粒制剂中测量了HO酶的活性。 UVA照射后至少3天，HO酶的活性逐渐增加。但是，本构性和UVA辐射诱导的HO活性对注射特定HO抑制剂锡原卟啉（Sn [IV']原卟啉IX； SnPP）的小鼠的作用敏感。此外，我们观察到在注射SnPP的小鼠中，UVA辐射对UVB辐射或顺式-UCA的免疫保护作用被取消。因为SnPP注射不会影响正常的接触超敏反应反应性，但会抑制组成型HO酶的活性，因此看来只有可诱导的HO才具有调节免疫功能的作用。这个f

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