Ashman R F, Saxon A, Stevens R H
J Allergy Clin Immunol. 1980 Apr;65(4):242-56. doi: 10.1016/0091-6749(80)90151-7.
Immunoregulatory defects in patients can be assigned to B cells, T helper cells, or T suppressor cells by means of a modification of the in vitro PWM-stimulated Ig biosynthesis assay. When lymphocyte subpopulations from patient and normal are recombined, multiple internal comparisons within a single experiment reveal the functional activity of each subpopulation. By this technique we studied nine adult patients with acquired panhypogammaglobulinemia and one with isolated IgG deficiency. Low total Ig production by the B cell fraction was demonstrated in seven of the nine panhypogammaglobulinemic patients. In four of these seven, IgG and IgA secretion was markedly reduced compared with IgM. In the two patients with normal total Ig production, elevated IgM compensated for lower IgA and IgG. The one patient with no surface Ig+ cells had a B cell defect, but no T cell defect. Reduced T help and excessive T suppression characterized two of the four patients with the most severe B cell defects. Three patients were anergic by delayed hypersensitivity skin testing and failed to sensitize to DNCB, but the patient with the most severe T cell defects in vitro was not among them. One of these three patients showed a mild T cell help defect and suppressor excess and the other two had pure B cell defects. Thus, anergy and T regulator function were not correlated. In three instances where hypersuppression was more evident by adding patient unfractionated cells than by adding patient T cells, suppression by the T depleted fraction could be demonstrated. No cases of radiation-resistant T suppression were revealed among the seven patients tested. Subnormal total protein synthesis, noted in six of seven patients with low Ig production, was invariably less marked than the Ig defect and often affected both T and B cells. One additional patient with pure IgG deficiency of 2 yr duration was essentially normal in her in vitro lymphocyte function. The general applicability of this experimental design for analysis of positive or negative immunoregulatory abnormalities is emphasized.
通过改良体外PWM刺激的Ig生物合成试验，可将患者的免疫调节缺陷归因于B细胞、辅助性T细胞或抑制性T细胞。当将患者和正常人的淋巴细胞亚群重新组合时，单个实验中的多次内部比较可揭示每个亚群的功能活性。通过这项技术，我们研究了9例获得性全丙种球蛋白血症成年患者和1例孤立性IgG缺乏患者。9例全丙种球蛋白血症患者中有7例显示B细胞部分的总Ig产生量较低。在这7例患者中的4例中，与IgM相比，IgG和IgA分泌明显减少。在总Ig产生正常的2例患者中，升高的IgM补偿了较低的IgA和IgG。1例无表面Ig⁺细胞的患者存在B细胞缺陷，但无T细胞缺陷。4例B细胞缺陷最严重的患者中有2例表现为辅助性T细胞功能降低和抑制性T细胞功能亢进。3例患者通过迟发型超敏皮肤试验呈无反应性，且对DNCB不敏感，但体外T细胞缺陷最严重的患者不在其中。这3例患者中有1例表现出轻度的辅助性T细胞功能缺陷和抑制性T细胞功能亢进，另外2例有单纯的B细胞缺陷。因此，无反应性与T调节功能无关。在3例中，加入未分离的患者细胞比加入患者T细胞时超抑制现象更明显，可证明T细胞耗竭部分具有抑制作用。在检测的7例患者中未发现抗辐射性T抑制的病例。7例Ig产生量低的患者中有6例总蛋白合成低于正常，其程度总是比Ig缺陷轻，且常同时影响T细胞和B细胞。1例持续2年的单纯IgG缺乏的额外患者，其体外淋巴细胞功能基本正常。强调了这种实验设计在分析免疫调节异常的阳性或阴性方面的普遍适用性。
