Zamansky G B, Minka D F, Deal C L, Hendricks K
J Immunol. 1985 Mar;134(3):1571-6.
To investigate the role of DNA damage in the pathogenesis of systemic lupus erythematosus (SLE), we studied the ability of skin fibroblasts derived from SLE patients to recover from ultraviolet (UV) light radiation of varying wavelengths. Four of five SLE cell strains were more sensitive to UV-C (254 nm), sun lamp, and UV-A (320 to 400 nm) light than were normal cells. SLE cellular recovery was most sensitive to broad spectrum, long wavelength light. This hypersensitivity did not appear to result from the UV light activation of a clastogenic factor. Experiments which examined the DNA repair capacity of irradiated cells indicated that SLE fibroblasts may be able to excise certain DNA lesions as well as normal cells. The mechanisms responsible for the hypersensitivity of SLE cells remain under investigation.
为了研究DNA损伤在系统性红斑狼疮(SLE)发病机制中的作用,我们研究了来自SLE患者的皮肤成纤维细胞从不同波长紫外线(UV)辐射中恢复的能力。五株SLE细胞株中有四株对UV-C(254nm)、太阳灯和UV-A(320至400nm)光比正常细胞更敏感。SLE细胞恢复对广谱长波长光最为敏感。这种超敏反应似乎不是由致裂因子的紫外线激活引起的。检测受辐照细胞DNA修复能力的实验表明,SLE成纤维细胞可能能够像正常细胞一样切除某些DNA损伤。SLE细胞超敏反应的机制仍在研究中。