Herrod H G, Buckley R H
J Clin Invest. 1979 May;63(5):868-76. doi: 10.1172/JCI109386.
A plaque assay that detects human mononuclear blood cells producing immunoglobulin (Ig)M antibody to sheep erythrocytes was investigated for its usefulness in studying B-cell activation and regulation in 24 patients with humoral immunodeficiency. Cells from 3 of 15 patients with common variable agammaglobulinemia produced some plaques (range 40--160/10(6) cells; normal range 80--1240/10(6)), but those from the other 12, from all 7 with x-linked agammaglobulinemia and from the 2 with x-linked immunodeficiency with hyper-IgM failed to produce any detectable plaques. In co-cultures of patient and normal cells a very good correlation was seen between results of the plaque assay and an IgM biosynthesis assay in detecting excessive suppressor cell activity. Cells from 7 of 15 common variable agammaglobulinemics, from 3 of 7 x-linked agammaglobulinemics, and from both patients with hyper-IgM caused significant suppression of IgM biosynthesis and(or) plaque formation by normal cells. The observations in the last two groups and discordance for excess suppressor activity in identical twins with common variable agammaglobulinemia suggest that the activity develops secondarily to whatever their primary defects may be. Culturing non-T cells from common variable agammaglobulinemics exhibiting excessive suppressor cell activity with normal T cells resulted in plaque formation in four of five patients so studied; in all five the suppressor activity was found in the T-cell population. The availability of a plaque assay for the study of blood cells from immunodeficient patients provides a new probe to examine the cellular nature of such defects.
我们研究了一种噬斑测定法，该方法用于检测产生抗绵羊红细胞免疫球蛋白（Ig）M抗体的人单核血细胞，以评估其在研究24例体液免疫缺陷患者B细胞活化和调节方面的实用性。15例常见变异型无丙种球蛋白血症患者中有3例的细胞产生了一些噬斑（范围为40 - 160/10⁶细胞；正常范围为80 - 1240/10⁶），但其他12例患者、所有7例X连锁无丙种球蛋白血症患者以及2例伴有高IgM的X连锁免疫缺陷患者的细胞均未产生任何可检测到的噬斑。在患者细胞与正常细胞的共培养中，噬斑测定结果与IgM生物合成测定结果在检测过度抑制细胞活性方面具有很好的相关性。15例常见变异型无丙种球蛋白血症患者中有7例的细胞、7例X连锁无丙种球蛋白血症患者中有3例的细胞以及2例高IgM患者的细胞均导致正常细胞的IgM生物合成和（或）噬斑形成受到显著抑制。最后两组的观察结果以及同卵双胞胎患常见变异型无丙种球蛋白血症时在过度抑制活性方面的不一致表明，这种活性是继发于其原发性缺陷的。对表现出过度抑制细胞活性的常见变异型无丙种球蛋白血症患者的非T细胞与正常T细胞进行培养，在5例接受研究的患者中有4例出现了噬斑形成；在所有5例患者中，抑制活性均存在于T细胞群体中。用于研究免疫缺陷患者血细胞的噬斑测定法为检查此类缺陷的细胞本质提供了一种新的手段。
