Metzger R, Melmer G, Schondelmaier S, Heckl-Ostreicher B, Nerl C, Pechhold K, Epplen J T, Kabelitz D
Institut für Immunologie, Universität Heidelberg, Germany.
Scand J Immunol. 1993 Feb;37(2):245-50. doi: 10.1111/j.1365-3083.1993.tb01762.x.
We investigated the in vitro responsiveness of peripheral blood lymphocytes from two patients with T-cell chronic lymphocytic leukaemia (T-CLL) to Staphylococcus aureus enterotoxin (SE) superantigens. T-cell receptor (TcR) alpha beta (V beta 7.1)-expressing CD4+ leukaemic T cells from patient HE (white blood cell count 480,000/microliters) proliferated in response to SEA and, only at 1000-fold higher concentrations, to SEB, SED, and SEE. CD4+CD8+ TcR alpha beta (V beta 12.1)-expressing leukaemic T cells from patient KO (white blood cell count 120,000/microliters) were activated by SEB but not by the other tested SEs. In both instances, the activation of leukaemic T cells by SE was dependent on the presence of HLA-DR+ cells. Southern blot analysis of TcR beta gene rearrangement confirmed that the proliferating cells were derived from the leukaemic T-cell clone and not from contaminating normal T cells. These data indicate that leukaemic T cells from patients with T-CLL exert a clonally variable responsiveness to SE superantigens. We conclude that recognition of specific antigen and subsequent signal transduction can be initiated via the TcR of leukaemic T-CLL cells.
我们研究了两名T细胞慢性淋巴细胞白血病(T-CLL)患者外周血淋巴细胞对金黄色葡萄球菌肠毒素(SE)超抗原的体外反应性。来自患者HE(白细胞计数480,000/微升)的表达T细胞受体(TcR)αβ(Vβ7.1)的CD4 +白血病T细胞对SEA有增殖反应,并且仅在浓度高1000倍时,对SEB、SED和SEE有反应。来自患者KO(白细胞计数120,000/微升)的表达CD4 + CD8 + TcRαβ(Vβ12.1)的白血病T细胞被SEB激活,但未被其他测试的SE激活。在这两种情况下,SE对白血病T细胞的激活都依赖于HLA-DR +细胞的存在。TcRβ基因重排的Southern印迹分析证实,增殖细胞来源于白血病T细胞克隆,而非来自污染的正常T细胞。这些数据表明,T-CLL患者的白血病T细胞对SE超抗原表现出克隆可变的反应性。我们得出结论,白血病T-CLL细胞可通过TcR启动对特定抗原的识别及随后的信号转导。