Carlsson R, Hedlund G, Sjögren H O
Scand J Immunol. 1987 Jan;25(1):11-9. doi: 10.1111/j.1365-3083.1987.tb01041.x.
Human mononuclear cells stimulated with staphylococcal enterotoxin A (SEA) for 2-6 days significantly suppress [3H]thymidine incorporation and reduce the levels of interleukin 2 (IL-2) and interferon (IFN) in culture medium when added to fresh, polyclonally activated mononuclear cells. The inhibitory capacity of the cells correlates well with the expression of IL-2 receptors. Lymphocytes obtained 3 days after stimulation with SEA, when the IL-2 receptor expression is high, are more potent inhibitors than cells obtained 2, 6, 11 or 14 days after stimulation, when the IL-2 receptors are less expressed on lymphocytes. T4+ and T8+ cells were both found to be inhibitory. Irradiation of the cells with 15 Gy before stimulation with SEA reduced but did not eliminate their suppressive capacity. The expression of the IL-2 receptor was lower in the irradiated cells. Irradiation or mitomycin-C treatment of cells after 3 and 5 days of SEA exposure had no effect on their inhibitory capacities. Pretreatment of the cells with IL-2 could partially reverse their suppressive effect on recorded IL-2 levels of stimulated fresh cultures. A complete reversal was obtained with the anti-Tac monoclonal antibody, which binds to the IL-2 receptor. The collective data show that the SEA-induced suppression of IL-2 activity in lymphocyte culture medium is not due to a suppression of the IL-2 production but rather depends on depletion of IL-2 due to absorption of IL-2 from the culture medium.
用葡萄球菌肠毒素A(SEA)刺激2 - 6天的人单核细胞,当添加到新鲜的、多克隆激活的单核细胞中时,会显著抑制[3H]胸腺嘧啶核苷掺入,并降低培养基中白细胞介素2(IL - 2)和干扰素(IFN)的水平。细胞的抑制能力与IL - 2受体的表达密切相关。在SEA刺激3天后获得的淋巴细胞,此时IL - 2受体表达较高,比在刺激后2、6、11或14天获得的细胞(此时淋巴细胞上IL - 2受体表达较少)是更强的抑制剂。发现T4 +和T8 +细胞均具有抑制作用。在用SEA刺激前用15 Gy照射细胞,可降低但不能消除其抑制能力。照射细胞中IL - 2受体的表达较低。在SEA暴露3天和5天后对细胞进行照射或丝裂霉素 - C处理,对其抑制能力没有影响。用IL - 2预处理细胞可部分逆转其对记录的刺激新鲜培养物中IL - 2水平的抑制作用。用与IL - 2受体结合的抗Tac单克隆抗体可实现完全逆转。总体数据表明,SEA诱导的淋巴细胞培养基中IL - 2活性的抑制不是由于IL - 2产生的抑制,而是取决于由于从培养基中吸收IL - 2导致的IL - 2消耗。