Kripke M L, McClendon E
J Immunol. 1986 Jul 15;137(2):443-7.
Exposure of mice to UVB radiation produces a highly selective, systemic immunosuppression associated with the appearance of suppressor T lymphocytes. Suppression of delayed hypersensitivity to hapten-coupled syngeneic cells has been shown to result from an altered distribution of antigen-presenting cells. The purpose of this study was to determine whether an alteration in the activity of antigen-presenting cells could account for the systemic suppression of contact hypersensitivity (CHS) by UVB radiation. Fluorescein isothiocyanate (FITC) was used for contact sensitization because it uses different antigen-presenting cells than does oxazolone to induce CHS. Our previous studies demonstrated that CHS to oxazolone was suppressed by UVB irradiation. In these studies, we show that exposure of mice to UVB radiation before epicutaneous application of FITC onto unirradiated skin markedly decreased the CHS response to FITC painted on unexposed ears. Cyclophosphamide-sensitive suppressor T cells were detectable in the spleens of mice exhibiting decreased CHS. The antigen-presenting activity of cells in lymph nodes draining the site of epicutaneous sensitization (DLN cells) was assessed by injecting them into the hind footpads of syngeneic recipients and measuring the CHS response to FITC 6 days later. Viable DLN cells from UVB-irradiated, FITC-sensitized mice were equal to those from unirradiated, FITC-sensitized mice in their ability to induce CHS in normal recipients. No sensitization resulted when killed DLN cells were used for immunization, indicating that sensitization was not caused by reprocessing of antigen by host cells. We conclude that impairment of the CHS reaction in UVB-irradiated mice does not appear to be blocked at an initial step of antigen uptake, processing, or presentation, but must be impaired at some other step in the immunologic pathway.
将小鼠暴露于中波紫外线（UVB）辐射下会产生一种高度选择性的全身性免疫抑制，这与抑制性T淋巴细胞的出现有关。对与半抗原偶联的同基因细胞的迟发型超敏反应的抑制已被证明是由于抗原呈递细胞分布的改变所致。本研究的目的是确定抗原呈递细胞活性的改变是否可以解释UVB辐射对接触性超敏反应（CHS）的全身性抑制作用。异硫氰酸荧光素（FITC）用于接触致敏，因为它与恶唑酮相比，诱导CHS时使用不同的抗原呈递细胞。我们之前的研究表明，UVB照射可抑制对恶唑酮的CHS。在这些研究中，我们发现，在将FITC经皮应用于未照射皮肤之前，先将小鼠暴露于UVB辐射下，可显著降低对涂于未暴露耳部的FITC的CHS反应。在CHS降低的小鼠脾脏中可检测到对环磷酰胺敏感的抑制性T细胞。通过将致敏部位引流淋巴结中的细胞（DLN细胞）注射到同基因受体的后足垫中，并在6天后测量对FITC 的CHS反应，来评估其抗原呈递活性。来自UVB照射、FITC致敏小鼠的活DLN细胞在诱导正常受体CHS方面的能力与来自未照射、FITC致敏小鼠的细胞相当。当使用经杀死的DLN细胞进行免疫时，未产生致敏，这表明致敏不是由宿主细胞对抗原的再加工引起的。我们得出结论，UVB照射小鼠中CHS反应的受损似乎不是在抗原摄取、加工或呈递的初始步骤被阻断，而是在免疫途径的其他某个步骤受损。
