Effect of local ultraviolet irradiation on infections of mice with Candida albicans, Mycobacterium bovis BCG, and Schistosoma mansoni.
Effect of local ultraviolet irradiation on infections of mice with Candida albicans, Mycobacterium bovis BCG, and Schistosoma mansoni.
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局部紫外线照射对小鼠白色念珠菌、牛分枝杆菌卡介苗和曼氏血吸虫感染的影响。
DOI：
10.1111/1523-1747.ep12611853
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发表时间：
1992
期刊：
影响因子：
--
通讯作者：
Kripke,ML
中科院分区：
文献类型：
--
作者：
Jeevan,A;Evans,R;Brown,EL;Kripke,ML
在这项研究中，我们调查了是否给予小鼠紫外线（UV）-B（280-320 nm）辐射的剂量足以改变皮肤免疫细胞和损害诱导的接触性超敏反应也会削弱抵抗感染剂管理的紫外线照射的网站。C3 H小鼠连续4天暴露于来自FS 40日光灯的400 J/m2 UVR。在最后一次紫外线照射后，立即给各组小鼠皮下注射白色念珠菌，皮内注射卡介苗（BCG），或在紫外线照射的皮肤上感染曼氏血吸虫。诱导对C.通过足垫肿胀评估，白色念珠菌和卡介苗不受紫外线照射的影响。然而，从BCG感染小鼠的淋巴器官中回收的活分枝杆菌的数量在紫外线照射的动物中显著增加超过2个月。低剂量紫外线照射感染部位皮肤不影响S.从6周前感染尾蚴的小鼠的内脏中可回收的曼氏寄生虫。我们的结论是，紫外线辐射的能力，损害细胞介导的免疫力的发展，在紫外线照射的网站引入的抗原是不普遍的，并取决于特定的抗原管理。我们推测表皮朗格汉斯细胞作为主要抗原呈递细胞参与细胞介导的免疫诱导可能是决定特定免疫应答是否会受到局部UV照射影响的关键因素。
In this study, we investigated whether mice given ultraviolet (UV)-B (280-320 nm) radiation in doses sufficient to alter cutaneous immune cells and impair the induction of contact hypersensitivity would also have impaired resistance to infectious agents administered at the site of UV irradiation. C3H mice were exposed to 400 J/m2UVR from FS40 sunlamps on four consecutive days. Immediately after the last UV treatment, groups of mice were injected subcutaneously withCandida albicans, injected intradermally (ID) withMycobacterium bovisbacillus Calmette-Guerin (BCG), or infected Percutaneously withSchistosoma mansoniin UV-irradiated skin. The induction of the delayed hypersensitivity response toC. albicansand BCG, as assessed by footpad swelling, was unaffected by UV irradiation. However, the number of viable mycobacteria recovered from the lymphoid organs of BCG-infected mice was increased significantly in the UV-irradiated animals for a period of more than 2 months. Low-dose UV irradiation of the skin at the site of infection did not influence the number ofS. mansoniparasites recoverable from the internal organs of mice that had been infected with cercariae percutaneously 6 weeks earlier. We conclude that the ability of UV radiation to impair the development of cell-mediated immunity to antigens introduced in a UV-irradiated site is not universal and depends on the particular antigen administered. We hypothesize that the involvement of epidermal Langerhans cells as the primary antigen-presenting cells in the induction of cell-mediated immunity may be the critical factor in determining whether a particular immune response will be affected by local UV irradiation.