Noonan F P, Bucana C, Sauder D N, De Fabo E C
J Immunol. 1984 May;132(5):2408-16.
We previously reported that broad band UV radiation or narrow bands of UV (Hbw 3 nm) of wavelengths 250 to 320 nm cause a systemic suppression of contact hypersensitivity (CHS) in mice, observed when the contact sensitizer is applied to a nonirradiated site. To determine if this effect is associated with UV-induced alterations in epidermal Langerhans cell (LC) numbers and morphology, we performed the following study. LC were identified by ATPase staining of EDTA-separated epidermal sheets. Electron microscope studies confirmed that this method was a satisfactory indicator of the presence of LC; we found no evidence for LC which did not stain for ATPase in either irradiated or unirradiated epidermis. Mice were irradiated on the back with narrow band UV of peak wavelength 270, 290, or 320 nm. The irradiated skin was excised 24 hr later and was stained as described. The number of LC with ATPase staining dendrites and the number of nondendritic LC were enumerated. We found that UV radiation of 270 or 290 nm caused 1) an alteration in LC morphology (loss of dendrites) and 2) a decrease in the total number of epidermal LC. Both effects occurred in a dose-dependent fashion. Previously, these same wavelengths of narrow band UV, but at higher doses, had been shown to cause systemic suppression of CHS. In this study, the doses of 270 or 290 nm UV that resulted in the decreased LC numbers and alterations in LC morphology described above were insufficient to cause systemic suppression of CHS. The converse was found if the irradiating waveband of UV had a peak at 320 nm. A dose of 320 nm UV that caused 50% systemic suppression of CHS had no effect on either the number or the morphology of LC at the site of irradiation. In addition, the number and morphology of LC were unaffected in the ventral epidermis (site of contact sensitization) of mice that had been previously irradiated on the back with a systemically suppressive dose of UV. We conclude: (a) UV-induced alterations in the number and morphology of LC at the site of irradiation are not necessary for the generation of systemic suppression of CHS by UV radiation; this indicates that the initial UV-absorbing event triggering systemic suppression is neither a loss of, nor morphologic alterations to, LC at the irradiation site. (b) A systemic effect of UV radiation on the number and morphology of LC at the unirradiated site of contact sensitization does not occur, and thus is not responsible for the UV-induced systemic suppression of CHS by UV radiation.
我们之前报道过，波长为250至320nm的宽带紫外线辐射或窄带紫外线（半高宽3nm）会导致小鼠接触性超敏反应（CHS）出现全身性抑制，这种抑制在将接触致敏剂应用于未受辐射部位时即可观察到。为了确定这种效应是否与紫外线诱导的表皮朗格汉斯细胞（LC）数量和形态改变有关，我们进行了以下研究。通过对EDTA分离的表皮片进行ATP酶染色来鉴定LC。电子显微镜研究证实，该方法是LC存在的一个令人满意的指标；我们发现在受辐射或未受辐射的表皮中，未发现未被ATP酶染色的LC。用峰值波长为270、290或320nm的窄带紫外线对小鼠背部进行辐射。24小时后切除受辐射的皮肤并按上述方法进行染色。对具有ATP酶染色树突的LC数量和非树突状LC数量进行计数。我们发现，270或290nm的紫外线辐射会导致：1）LC形态改变（树突丧失）；2）表皮LC总数减少。这两种效应均呈剂量依赖性。此前，相同波长的窄带紫外线，但剂量更高时，已被证明会导致CHS的全身性抑制。在本研究中，导致上述LC数量减少和LC形态改变的270或290nm紫外线剂量不足以引起CHS的全身性抑制。如果紫外线的辐射波段峰值在320nm，则情况相反。导致CHS全身性抑制50%的320nm紫外线剂量对受辐射部位的LC数量或形态均无影响。此外，之前背部接受过全身性抑制剂量紫外线辐射的小鼠，其腹部表皮（接触致敏部位）的LC数量和形态未受影响。我们得出以下结论：（a）紫外线诱导受辐射部位的LC数量和形态改变并非紫外线辐射产生CHS全身性抑制所必需；这表明触发全身性抑制的初始紫外线吸收事件既不是受辐射部位LC的丧失，也不是其形态改变。（b）紫外线辐射对未受辐射的接触致敏部位的LC数量和形态没有全身性影响，因此也不是紫外线辐射诱导CHS全身性抑制产生的原因。
