Skov L, Baadsgaard O
Department of Dermatology, University of Copenhagen, Hellerup, Denmark.
Br J Dermatol. 1996 May;134(5):824-30.
In this study we tested the capacity of ultraviolet B (UVB)-irradiated major histocompatibility complex (MHC) class II+ keratinocytes, monocytes and dendritic cells to activate T cells in the presence of Staphylococcus enterotoxin B. We demonstrated that UVB irradiation of MHC class II+ keratinocytes does not change their capacity to activate T cells in the presence of Staphylococcus enterotoxin B. In contrast, UVB irradiation of antigen-presenting cells decreases their capacity to activate T cells. This differential capacity to activate T cells after UVB irradiation was not due to factors released from UVB-irradiated cells. The interferon-gamma induced upregulation of HLA-DR and intercellular adhesion molecule-1 on keratinocytes does not seem to be the only explanation, since UVB irradiation decreased the accessory cell function of interferon-gamma pretreated monocytes. Differential requirements for and UVB regulation of costimulatory molecules may be involved, since blocking of the B7/CD28 pathway affects the capacity of dendritic cells but not keratinocytes to activate T cells in the presence of Staphylococcus enterotoxin B. Thus, MHC class II+ keratinocytes in the presence of superantigens released from staphylococci may activate T cells and maintain inflammation despite UVB treatment.
在本研究中,我们测试了紫外线B(UVB)照射的主要组织相容性复合体(MHC)II类阳性角质形成细胞、单核细胞和树突状细胞在存在葡萄球菌肠毒素B的情况下激活T细胞的能力。我们证明,在存在葡萄球菌肠毒素B的情况下,UVB照射MHC II类阳性角质形成细胞不会改变其激活T细胞的能力。相比之下,UVB照射抗原呈递细胞会降低其激活T细胞的能力。UVB照射后激活T细胞的这种差异能力并非由于UVB照射细胞释放的因子所致。干扰素-γ诱导角质形成细胞上HLA-DR和细胞间黏附分子-1的上调似乎并非唯一解释,因为UVB照射降低了干扰素-γ预处理单核细胞的辅助细胞功能。可能涉及共刺激分子的不同需求和UVB调节,因为阻断B7/CD28途径会影响树突状细胞在存在葡萄球菌肠毒素B的情况下激活T细胞的能力,但不影响角质形成细胞。因此,在存在葡萄球菌释放的超抗原的情况下,MHC II类阳性角质形成细胞可能会激活T细胞并维持炎症,尽管进行了UVB治疗。