Walunas T L, Bluestone J A
The Committee on Immunology and the Ben May Institute for Cancer Research, The University of Chicago, IL 60637, USA.
J Immunol. 1998 Apr 15;160(8):3855-60.
Cytotoxic T lymphocyte Ag-4 (CTLA-4; CD152) is an important T cell regulatory molecule. In vitro experiments have shown that the blockade of signals through CTLA-4 augments T cell expansion, while CTLA-4 cross-linking results in decreased T cell proliferation due to decreased IL-2 production. However, less is known about the role of CTLA-4 in regulating an ongoing immune response. In this study, we examined the role of CTLA-4 in the expansion, decline, tolerization, and differentiation of T cells following treatment with staphylococcal enterotoxin B (SEB). Anti-CTLA-4 treatment resulted in increased numbers of SEB-reactive T cells and blockade of subsequent tolerance induction. Further examination of the SEB-reactive cells from anti-CTLA-4-treated mice demonstrated that both the CD4+ and CD8+ Vbeta8+ T cells produced IL-4, providing evidence that not only do signals through CTLA-4 regulate T cell-tolerizing events, but they also play an important role in the differentiation of T cells in vivo.
细胞毒性T淋巴细胞抗原4（CTLA-4；CD152）是一种重要的T细胞调节分子。体外实验表明，通过CTLA-4阻断信号可增强T细胞扩增，而CTLA-4交联则由于白细胞介素-2产生减少导致T细胞增殖降低。然而，关于CTLA-4在调节正在进行的免疫反应中的作用，人们了解较少。在本研究中，我们研究了CTLA-4在金黄色葡萄球菌肠毒素B（SEB）处理后T细胞的扩增、衰退、耐受形成及分化中的作用。抗CTLA-4治疗导致SEB反应性T细胞数量增加，并阻断了随后的耐受诱导。对来自抗CTLA-4治疗小鼠的SEB反应性细胞的进一步检测表明，CD4+和CD8+ Vβ8+ T细胞均产生白细胞介素-4，这表明不仅通过CTLA-4的信号调节T细胞耐受形成事件，而且它们在体内T细胞分化中也发挥重要作用。
