Analysis of the mechanism of unresponsiveness produced by haptens painted on skin exposed to low dose ultraviolet radiation.
Analysis of the mechanism of unresponsiveness produced by haptens painted on skin exposed to low dose ultraviolet radiation.
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DOI：
10.1084/jem.158.3.781
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发表时间：
1983-09-01
期刊：
影响因子：
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通讯作者：
Streilein JW
中科院分区：
文献类型：
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作者：
Elmets CA;Bergstresser PR;Tigelaar RE;Wood PJ;Streilein JW
对小鼠体壁皮肤进行急性、低剂量的紫外线 B 辐射，然后局部应用 DNFB，会产生抗原特异性无反应状态。这种状态至少部分是由 Lyt-1+ T 细胞维持的，Lyt-1+ T 细胞通过损害接触性超敏反应的诱导期而导致无反应。缺乏能够在免疫效应阶段发挥作用的抑制细胞表明，源自皮肤的耐受性信号建立的抑制网络是不完整的，并且可能与全身施用耐受原诱导的网络不同。有人提出，紫外线辐射通过损害常驻朗格汉斯细胞的抗原呈递潜力来产生其作用，在朗格汉斯细胞不存在的情况下，半抗原衍生的角质形成细胞（或其产物）能够传递耐受性信号。
Acute, low dose ultraviolet B radiation of murine body wall skin followed by local application of DNFB produces a state of antigen- specific unresponsiveness. This state is maintained at least in part by an Lyt-1+ T cell that effects unresponsiveness by impairing the induction phase of contact hypersensitivity. The absence of suppressor cells capable of acting at the effector stage of immunity suggests that tolerogenic signals derived from the skin establish suppressor networks that are incomplete and perhaps different from networks that are induced by systemic administration of tolerogens. It is proposed that ultraviolet radiation produces its effects by impairing the antigen- presenting potential of resident Langerhans cells in whose absence hapten-derivatized keratinocytes (or their products) are able to deliver a tolerogenic signal.