Smith J B, Knowlton R P
J Immunol. 1979 Jul;123(1):419-22.
Co-culture of autologous T and mitomycin-C treated B cells results in increased DNA synthesis in the responding T cells. T cells thus activated in AMLC exerted suppressive effects on both the proliferative and cytotoxic responses of fresh unstimulated T cells to allogeneic cells in MLC. The suppressor cells generated are sensitive to treatment with mitomycin-C. AMLC-activated cells treated with mitomycin-C failed to suppress both cytotoxicity and proliferation in fresh primary MLC. It appears that the AMLC reaction reflects an immunologic homeostatic mechanism. Since this reaction is defective in patients with CLL and SLE and the homologous mouse syngeneic MLC is defective in NZB mice, the failure of this T-B interaction may be related to the pathogenesis of certain lymphoproliferative and autoimmune disorders.
自体T细胞与丝裂霉素C处理的B细胞共培养可导致反应性T细胞中DNA合成增加。在急性髓细胞白血病细胞（AMLC）中如此激活的T细胞对新鲜未刺激的T细胞在混合淋巴细胞培养（MLC）中对同种异体细胞的增殖和细胞毒性反应均产生抑制作用。所产生的抑制细胞对丝裂霉素C处理敏感。用丝裂霉素C处理的AMLC激活细胞在新鲜原代MLC中未能抑制细胞毒性和增殖。看来AMLC反应反映了一种免疫稳态机制。由于该反应在慢性淋巴细胞白血病（CLL）和系统性红斑狼疮（SLE）患者中存在缺陷，且同源小鼠同基因MLC在新西兰黑（NZB）小鼠中存在缺陷，这种T - B相互作用的失败可能与某些淋巴增殖性疾病和自身免疫性疾病的发病机制有关。
