Roberts A I, Blumberg R S, Christ A D, Brolin R E, Ebert E C
Department of Medicine, UMDNJ-Robert Wood Johnson Medical School, New Brunswick, NJ 08903, USA.
Immunology. 2000 Oct;101(2):185-90. doi: 10.1046/j.1365-2567.2000.00088.x.
In food poisoning, Staphylococcus aureus secretes staphylococcal enterotoxin B (SEB), a superantigen that causes intense T-cell proliferation and cytotoxicity. The effects of SEB on lytic activity by human intestinal intraepithelial lymphocytes (IEL) were investigated. Jejunal IEL, from morbidly obese individuals undergoing gastric bypass operations, were tested for SEB-induced cytotoxicity against C1R B-lymphoblastoid cells, HT-29 adenocarcinoma cells, or CD1d-transfected cells using the 51Cr-release assay. Fas and Fas ligand expression were detected by immunofluorescence and flow cytometry and soluble ligand by enzyme-linked immunosorbent assay (ELISA). In the presence of SEB, IEL became potently cytotoxic against C1R cells and interferon-gamma (IFN-gamma)-precultured HT-29 cells, causing 55+/-10% and 31+/-6% lysis, respectively, greater than that by phytohaemagglutinin (PHA)-, interleukin-2 (IL-2)-, or anti-T-cell receptor (TCR)-activated IEL. SEB-stimulated peripheral blood (PB) CD8+ T cells lysed similar numbers of C1R cells but fewer HT-29 cells (53+/-13% and 8+/-5%, respectively). IEL killing of C1R cells involved interaction of major histocompatibility complex (MHC) class II with TCR, CD2 with CD58, and CD11a with CD54, and was perforin mediated. SEB-induced IEL lysis of HT-29 cells, in contrast, was caused by an unknown target cell structure, not MHC class II or CD1d, and resulted from a combination of perforin and Fas-mediated events. The potent cytotoxic activities of IEL promoted by SEB utilize two different mechanisms, depending on the surface receptors expressed by the target cells.
在食物中毒中，金黄色葡萄球菌分泌葡萄球菌肠毒素B（SEB），这是一种超抗原，可引起强烈的T细胞增殖和细胞毒性。研究了SEB对人肠道上皮内淋巴细胞（IEL）裂解活性的影响。使用51Cr释放试验，对接受胃旁路手术的病态肥胖个体的空肠IEL进行测试，检测其对C1R B淋巴母细胞、HT - 29腺癌细胞或CD1d转染细胞的SEB诱导的细胞毒性。通过免疫荧光和流式细胞术检测Fas和Fas配体的表达，并通过酶联免疫吸附测定（ELISA）检测可溶性配体。在SEB存在的情况下，IEL对C1R细胞和干扰素-γ（IFN - γ）预培养的HT - 29细胞具有强大的细胞毒性，分别导致55±10%和31±6%的细胞裂解，高于植物血凝素（PHA）、白细胞介素-2（IL - 2）或抗T细胞受体（TCR）激活的IEL。SEB刺激的外周血（PB）CD8 + T细胞裂解的C1R细胞数量相似，但HT - 29细胞较少（分别为53±13%和8±5%）。IEL对C1R细胞的杀伤涉及主要组织相容性复合体（MHC）II类与TCR、CD2与CD58以及CD11a与CD54的相互作用，并且是穿孔素介导的。相比之下，SEB诱导的IEL对HT - 29细胞的裂解是由未知的靶细胞结构引起的，而非MHC II类或CD1d，并且是穿孔素和Fas介导事件共同作用的结果。SEB促进的IEL的强大细胞毒性活性利用两种不同机制，这取决于靶细胞表达的表面受体。
