Potts R C, Sherif M M, Robertson A J, Gibbs J H, Brown R A, Beck J S
Scand J Immunol. 1981 Sep;14(3):269-80. doi: 10.1111/j.1365-3083.1981.tb00564.x.
The sera of ten Egyptian man with long-standing lepromatous leprosy (LL) (mean duration 17.4 years) that had failed to respond to dapsone treatment were shown to inhibit mitogen stimulation responses of normal human lymphocytes. When first tested, the sera partly inhibited the response to phytohaemagglutinin (PHA) and pokeweed mitogen and virtually abolished that to concanavalin A (Con A): after repeated freezing and thawing, the Con A inhibition had disappeared, whereas the PHA response was still partly inhibited. The inhibitory serum factor(s) had similar actions on lymphocytes from each of six normal donors. Although the sera varied in potency, they showed similar dose-response curves when tested against lymphocytes from a single donor. The principal action of the sera was to reduce the number of cells responding to mitogen, without modifying the kinetics of recruitment or rate of volume growth during G1-phase in those cells that were unaffected by the inhibitory substances(s). Study of PHA dose-response curves and of the effect of delayed addition of LL serum suggested that the serum factor(s) act by diminishing the responsiveness of the cells, rather than by reducing the concentrations of free mitogen or by blocking cell membrane mitogen receptors. The serum from one apparently healthy attendant, who had nursed leprosy patients for 30 years but who did not have leprosy or other chronic infective disease, inhibited completely stimulation by all three mitogens in a manner different from that of LL sera. Serum from the other 13 control patients did not modify the response of normal lymphocytes to stimulation by any of the three mitogens studied. It was concluded that the inhibitory factor(s) in the serum of patients with LL were a consequence of the disease and not of the environment in which the patients lived. Microscopy confirmed that the techniques used for recovery of the cultured cells did not introduce bias into the volume spectroscopy measurements.
十名长期患瘤型麻风（LL）（平均患病时长17.4年）且对氨苯砜治疗无反应的埃及男性患者的血清，被证明能抑制正常人淋巴细胞的丝裂原刺激反应。首次检测时，这些血清部分抑制了对植物血凝素（PHA）和商陆有丝分裂原的反应，并且几乎完全消除了对刀豆球蛋白A（Con A）的反应：反复冻融后，Con A抑制作用消失，而PHA反应仍受到部分抑制。这种抑制性血清因子对六名正常供体中每一位的淋巴细胞都有类似作用。尽管血清的效力各不相同，但在针对单一供体的淋巴细胞进行检测时，它们呈现出相似的剂量反应曲线。血清的主要作用是减少对丝裂原产生反应的细胞数量，而不会改变那些未受抑制物质影响的细胞在G1期的募集动力学或体积增长速率。对PHA剂量反应曲线以及延迟添加LL血清的效果的研究表明，血清因子的作用是降低细胞的反应性，而非降低游离丝裂原的浓度或阻断细胞膜丝裂原受体。一名显然健康的护理人员，他护理麻风患者30年，但自己没有患麻风病或其他慢性传染病，其血清以一种不同于LL血清的方式完全抑制了所有三种丝裂原的刺激作用。其他13名对照患者的血清并未改变正常淋巴细胞对所研究的三种丝裂原中任何一种刺激的反应。得出的结论是，LL患者血清中的抑制因子是疾病的结果，而非患者所处环境的结果。显微镜检查证实，用于回收培养细胞的技术并未在体积光谱测量中引入偏差。
