Fuller C L, Braciale V L
Department of Microbiology, Beirne B. Carter Center for Immunology Research, Health Sciences Center, University of Virginia, Charlottesville 22908, USA.
J Immunol. 1998 Nov 15;161(10):5179-86.
Upon encounter with its antigenic stimulus, CTL characteristically proliferate, produce cytokines, and lyse the Ag-presenting cell in an attempt to impede further infection. Superantigens are extremely efficient immunostimulatory proteins that promote high levels of proliferation and massive cytokine production in reactive T cells. We compared the activation of murine influenza-specific CD8+ CTL clones stimulated with either influenza peptide or the superantigen staphylococcus enterotoxin B (SEB). We found that influenza peptide/MHC and SEB appeared equally capable of eliciting proliferation and IFN-gamma production. However, while influenza peptide/MHC elicited both perforin- and Fas ligand (FasL)/Fas (CD95L/CD95)-mediated cytolytic mechanisms, SEB was unable to trigger perforin-mediated cytolysis or serine esterase release. Examination of intracellular Ca2+ mobilization events revealed that the ability to trigger intracellular Ca2+ flux was not comparable between influenza peptide and SEB. SEB stimulated only a small rise in levels of intracellular Ca2+, at times indistinguishable from background. These findings indicate that the short-term cytolytic potential of superantigen-activated CD8+ CTL clones appears to be restricted to FasL/Fas (CD95L/CD95) mediated cytolysis.
遇到抗原刺激后，细胞毒性T淋巴细胞（CTL）通常会增殖、产生细胞因子并裂解抗原呈递细胞，以试图阻止进一步感染。超抗原是极其有效的免疫刺激蛋白，可促进反应性T细胞的高水平增殖和大量细胞因子产生。我们比较了用流感肽或超抗原葡萄球菌肠毒素B（SEB）刺激的鼠源流感特异性CD8⁺CTL克隆的激活情况。我们发现，流感肽/MHC和SEB似乎同样能够引发增殖和干扰素-γ产生。然而，虽然流感肽/MHC引发了穿孔素和Fas配体（FasL）/Fas（CD95L/CD95）介导的细胞溶解机制，但SEB无法触发穿孔素介导的细胞溶解或丝氨酸酯酶释放。对细胞内Ca²⁺动员事件的检查表明，流感肽和SEB触发细胞内Ca²⁺通量的能力不可比。SEB仅刺激细胞内Ca²⁺水平小幅升高，有时与背景无明显差异。这些发现表明，超抗原激活的CD8⁺CTL克隆的短期细胞溶解潜力似乎仅限于FasL/Fas（CD95L/CD95）介导的细胞溶解。
