Gonzalo J A, Martinez C, Springer T A, Gutierrez-Ramos J C
Center for Blood Research, Harvard Medical School, Boston, MA 02115, USA.
Int Immunol. 1995 Oct;7(10):1691-8. doi: 10.1093/intimm/7.10.1691.
The response of T lymphocytes to superantigens requires expression of the appropriate TCR V beta gene products as well as the establishment of cellular interactions mediated by adhesion molecules. To study the role of intercellular adhesion molecule (ICAM)-1 in the response in vivo to superantigens, we have analyzed the effects induced by the bacterial superantigen Staphylococcus aureus enterotoxin B (SEB) in mice which have been made genetically deficient in ICAM-1. SEB treatment of wild-type mice causes proliferation, deletion and anergy of the SEB-reactive V beta 8+ T cell population. Here we show that cellular interactions mediated by ICAM-1 are not essential for the induction of anergy or for the deletion of CD4+ V beta 8+ or CD8+ V beta 8+ T cells, but are required for the proliferation of these peripheral T lymphocytes. This is the first demonstration in vivo that the absence of the co-stimulatory signals provided by the interaction of ICAM-1 with its specific ligands impairs the proliferation of SEB-reactive T cells. Interestingly, our study showed that SEB-induced proliferation of CD8+ V beta 8+ T cells from lymph nodes (not from spleen) is independent of the interactions mediated by ICAM-1.
T淋巴细胞对超抗原的应答需要表达适当的TCR Vβ基因产物，以及建立由黏附分子介导的细胞间相互作用。为了研究细胞间黏附分子（ICAM）-1在体内对超抗原应答中的作用，我们分析了细菌超抗原金黄色葡萄球菌肠毒素B（SEB）对ICAM-1基因缺陷小鼠的诱导效应。用SEB处理野生型小鼠会导致SEB反应性Vβ8 + T细胞群体的增殖、缺失和无反应性。在此我们表明，由ICAM-1介导的细胞间相互作用对于无反应性的诱导或CD4 + Vβ8 +或CD8 + Vβ8 + T细胞的缺失并非必需，但对于这些外周T淋巴细胞的增殖是必需的。这是首次在体内证明ICAM-1与其特异性配体相互作用所提供的共刺激信号缺失会损害SEB反应性T细胞的增殖。有趣的是，我们的研究表明，SEB诱导的来自淋巴结（而非脾脏）的CD8 + Vβ8 + T细胞的增殖独立于由ICAM-1介导的相互作用。
