Kim T Y, Kripke M L, Ullrich S E
Department of Immunology, University of Texas M.D. Anderson Cancer Center, Houston 77030.
J Invest Dermatol. 1990 Jan;94(1):26-32. doi: 10.1111/1523-1747.ep12873322.
Exposure of murine epidermal cells to UV radiation in vitro causes the release of immunoregulatory factors that mimic some of the immunosuppressive effects of in vivo UV irradiation. The purpose of this study was to investigate the spectrum of immune responses affected following i.v. injection of supernatants obtained from cultures of epidermal cells exposed in vitro to UV radiation. Treatment of primary epidermal cell cultures or transformed keratinocytes (Pam 212 cells) with UVB (280-320 nm) radiation caused the release of factors that suppressed the induction of delayed hypersensitivity to alloantigen and trinitrophenyl-modified self-antigens in syngeneic and allogeneic mice. Contrary to expectations, however, the injection of supernatants from UVB-irradiated epidermal cells had no effect on the induction of contact hypersensitivity to trinitrochlorobenzene. On the other hand, treatment of the keratinocytes with UVA radiation (320-400 nm, filtered to remove wavelengths in the UVB region) resulted in the release of a factor that suppressed contact but not delayed hypersensitivity. Neither the UVA-induced nor the UVB-induced suppressive factor inhibited the generation of an antibody response to sheep erythrocytes, indicating that, like the suppression that occurs after in vivo exposure to UV radiation, the suppression induced by factors from UV-irradiated keratinocytes is selective in nature. These data support the hypothesis that soluble keratinocyte-derived suppressive factors are involved in the induction of systemic immune suppression by UV radiation. In addition, they suggest that multiple suppressive factors, having different immunosuppressive properties, are produced by different wavelengths of UV radiation.
体外将小鼠表皮细胞暴露于紫外线辐射会导致免疫调节因子的释放,这些因子可模拟体内紫外线照射的一些免疫抑制作用。本研究的目的是调查静脉注射从体外暴露于紫外线辐射的表皮细胞培养物中获得的上清液后所影响的免疫反应谱。用UVB(280 - 320nm)辐射处理原代表皮细胞培养物或转化的角质形成细胞(Pam 212细胞)会导致因子释放,这些因子会抑制同基因和异基因小鼠对同种异体抗原和三硝基苯基修饰的自身抗原的迟发型超敏反应的诱导。然而,与预期相反,注射来自UVB照射的表皮细胞的上清液对三硝基氯苯接触性超敏反应的诱导没有影响。另一方面,用UVA辐射(320 - 400nm,过滤以去除UVB区域的波长)处理角质形成细胞会导致一种因子的释放,该因子抑制接触性超敏反应但不抑制迟发型超敏反应。UVA诱导的和UVB诱导的抑制因子均不抑制对绵羊红细胞的抗体反应的产生,这表明,与体内暴露于紫外线辐射后发生的抑制一样,紫外线照射的角质形成细胞产生的因子所诱导的抑制在本质上是选择性的。这些数据支持可溶性角质形成细胞衍生的抑制因子参与紫外线辐射诱导的全身免疫抑制的假说。此外,它们表明不同波长的紫外线辐射会产生具有不同免疫抑制特性的多种抑制因子。