Lisak R P, Laramore C, Levinson A I, Zweiman B, Moskovitz A R, Witte A
Neurology. 1984 Jun;34(6):802-5. doi: 10.1212/wnl.34.6.802.
Peripheral blood mononuclear cells of 15 of 20 patients with generalized myasthenia gravis synthesized antibodies to acetylcholine receptor (AChR) when the cells were stimulated in vitro with pokeweed mitogen. In contrast, mononuclear cells of 1 of 16 normal subjects synthesized detectable AChR antibodies. Peripheral blood mononuclear cells of five normal subjects were studied before and after putative suppressor T cells (OKT8+) were removed by a fluorescent activated cell sorter. Depletion of OKT8+ cells did not result in production of AChR antibodies, but pokeweed mitogen-induced polyclonal IgG synthesis and activation of B cells to form immunoglobulin-secreting cells (reverse hemolytic plaque assay) were increased. Therefore, failure of blood mononuclear cells of normal subjects to synthesize detectable anti-AChR in response to pokeweed mitogen is not due to suppression by OKT8+ cells.
20例全身性重症肌无力患者中有15例的外周血单个核细胞在体外用商陆有丝分裂原刺激时可合成抗乙酰胆碱受体(AChR)抗体。相比之下,16例正常受试者中有1例的单个核细胞可合成可检测到的AChR抗体。在用荧光激活细胞分选仪去除假定的抑制性T细胞(OKT8 +)之前和之后,对5例正常受试者的外周血单个核细胞进行了研究。去除OKT8 +细胞并未导致AChR抗体的产生,但商陆有丝分裂原诱导的多克隆IgG合成以及B细胞激活形成分泌免疫球蛋白的细胞(反向溶血空斑试验)增加。因此,正常受试者的血液单个核细胞对商陆有丝分裂原无反应而无法合成可检测到的抗AChR并非由于OKT8 +细胞的抑制作用。