Yee G K, Levy J G, Kripke M L, Ullrich S E
Department of Immunology, University of Texas, M.D. Anderson Cancer Center, Houston.
Cell Immunol. 1990 Apr 1;126(2):255-67. doi: 10.1016/0008-8749(90)90319-m.
The purpose of this study was to determine whether the ultraviolet (UV) radiation-induced systemic suppression of the immune response results from the release of soluble suppressor factors (TsF) by UV-induced suppressor T cells (UV Ts). Injecting a TsF-specific monoclonal antibody (B16G) significantly reduced the UV radiation-induced suppression of contact hypersensitivity (CHS). The transfer of spleen cells from the UV-irradiated, B16G-treated mice into normal recipients suppressed CHS in the recipients, indicating that while the suppression of CHS was reversed in the UV-irradiated, B16G-treated mice, suppressor cells were still present. Supernatants from cultures containing UV Ts were incubated on B16G-immunoadsorbent columns. The antibody-bound fraction (45- to 60-kDa, non-disulfide-linked proteins) suppressed CHS when injected into normal recipients. These results demonstrate that the B16G antibody reacts with TsF from UV Ts and suggest that B16G acts in vivo by inhibiting the activity of TsF. Thus, suppressor factors appear to play an essential role in the regulation of immune responses by UV Ts.
本研究的目的是确定紫外线（UV）辐射诱导的免疫反应全身性抑制是否源于紫外线诱导的抑制性T细胞（UV Ts）释放可溶性抑制因子（TsF）。注射TsF特异性单克隆抗体（B16G）可显著减轻紫外线辐射诱导的接触性超敏反应（CHS）抑制。将经紫外线照射、B16G处理的小鼠的脾细胞转移至正常受体中可抑制受体的CHS，这表明虽然经紫外线照射、B16G处理的小鼠中CHS的抑制作用得到逆转，但抑制性细胞仍然存在。将含有UV Ts的培养物的上清液在B16G免疫吸附柱上孵育。当注入正常受体时，抗体结合部分（45至60 kDa，非二硫键连接蛋白）可抑制CHS。这些结果表明，B16G抗体与UV Ts产生的TsF发生反应，并提示B16G在体内通过抑制TsF的活性发挥作用。因此，抑制因子似乎在UV Ts对免疫反应的调节中起重要作用。
