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紫外线照射对皮肤利什曼病发病机制的抑制作用。

Suppression of pathogenesis in cutaneous leishmaniasis by UV irradiation.

作者信息

Giannini M S

出版信息

Infect Immun. 1986 Mar;51(3):838-43. doi: 10.1128/iai.51.3.838-843.1986.

Abstract

The effects of suberythematous levels of UV-B radiation on the development of of cutaneous leishmaniasis were studied in B10.129(10M) mice. Doses of 15 mJ cm-2 UV-B applied locally to the injection site suppressed the development of skin lesions after the inoculation of Leishmania major promastigotes. The primary targets of UV-B radiation appeared to be host cells and not leishmanial parasites, because UV-B irradiation of parasites cultured in vitro did not affect their viability, but did kill host cells. Furthermore, the same numbers of parasites were recovered from skin at the injection site in both irradiated and control mice. UV-B irradiation abrogated the induction of contact hypersensitivity to dinitrofluorobenzene and also abrogated the induction of delayed-type hypersensitivity responses to leishmanial antigens. These results suggest that local perturbations in the functions of the skin-associated lymphoid tissue during the initial phases of leishmanial infection can profoundly influence immunological response and the subsequent development of clinical disease.

摘要

在B10.129(10M)小鼠中研究了亚红斑量UV-B辐射对皮肤利什曼病发展的影响。将15 mJ/cm²的UV-B剂量局部应用于注射部位,可抑制接种硕大利什曼原虫前鞭毛体后皮肤病变的发展。UV-B辐射的主要靶点似乎是宿主细胞而非利什曼原虫寄生虫,因为体外培养的寄生虫经UV-B照射后其活力不受影响,但会杀死宿主细胞。此外,在照射组和对照组小鼠的注射部位皮肤中回收的寄生虫数量相同。UV-B照射消除了对二硝基氟苯的接触性超敏反应的诱导,也消除了对利什曼原虫抗原的迟发型超敏反应的诱导。这些结果表明,在利什曼原虫感染的初始阶段,皮肤相关淋巴组织功能的局部扰动可深刻影响免疫反应及随后临床疾病的发展。

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Immunological unresponsiveness induced by ultraviolet radiation.紫外线辐射诱导的免疫无反应性。
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