Cell membrane is a major locus for ultraviolet B-induced alterations in accessory cells.
Cell membrane is a major locus for ultraviolet B-induced alterations in accessory cells.
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DOI：
10.1172/jci114600
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发表时间：
1990-05
期刊：
影响因子：
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通讯作者：
Jean Krutmann;Islam U. Khan;Robert S. Wallis;Fen Zhang;Elizabeth A. Rich;J. Ellner;C. A. Elmets
中科院分区：
文献类型：
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作者：
Jean Krutmann;Islam U. Khan;Robert S. Wallis;Fen Zhang;Elizabeth A. Rich;J. Ellner;C. A. Elmets
人血单核细胞的体外紫外线 B (UVB) 照射会抑制其抗原和丝裂原诱导的 T 细胞反应的辅助细胞功能。这些研究旨在表征 UVB 诱导的人类单核细胞辅助细胞功能缺陷的性质。受辐射的单核细胞缺乏作为 OKT3 诱导的 T 细胞激活的辅助细胞的能力。体外将单核细胞暴露于 100 J/m2 UVB 完全抑制 T 细胞增殖反应（51502 cpm，未 UVB 照射；302 cpm，UVB 照射）。对 UVB 改变的辅助信号的分析表明，受照射的单核细胞无法与 T 细胞上 CD3 抗原所附着的 OKT3 分子结合。通过将抗小鼠 IgG 连接到微量滴定孔底部来提供另一种结合 OKT3 分子的机制，完全恢复了辅助细胞功能。对缺陷的进一步表征表明，UVB 辐射不会耗尽受辐射单核细胞表面的 p72 Fc 受体。然而，UVB 暴露确实导致单核细胞膜 ICAM-1 表达出现剂量依赖性下降。有人提出，UVB 辐射会导致细胞膜内的变化，从而抑制单核细胞表达 T 细胞结合所需的选定分子的能力。
In vitro ultraviolet B (UVB) irradiation of human blood monocytes inhibits their accessory cell function for antigen- and mitogen-induced T cell responses. These studies were designed to characterize the nature of the UVB-induced defect in human monocyte accessory cell function. Irradiated monocytes were deficient in their ability to serve as accessory cells for OKT3-induced T cell activation. In vitro exposure of monocytes to 100 J/m2 UVB completely inhibited the T cell proliferative response (51502 cpm, non-UVB-irradiated; 302 cpm, UVB-irradiated). Analysis of the accessory signals altered by UVB indicated that irradiated monocytes were incapable of binding to OKT3 molecules attached to the CD3 antigen on T cells. Provision of an alternative mechanism for binding of OKT3 molecules by attaching anti-mouse IgG to the bottom of microtiter wells completely restored accessory cell function. Further characterization of the defect demonstrated that UVB radiation did not deplete p72 Fc receptors from the surface of irradiated monocytes. However, UVB exposure did produce a dose-dependent decrease in monocyte membrane expression of ICAM-1. It is proposed that UVB radiation leads to changes within the cell membrane that inhibit the ability of monocytes to express selected molecules necessary for binding of T cells.