Church J A, Nye C
Ann Allergy. 1982 Apr;48(4):199-204.
Suppressor cell dysfunction has been suggested as a cause of the heightened IgE responses seen in human atopic disease and allergy immunotherapy has been shown to be associated with the generation of antigen-specific suppressor cells. In an attempt to simulate immunotherapy, the in vitro effects of grass antigen exposure upon non-control subjects were treated with preincubation, concanavalin A or varying concentrations of a crude grass antigen preparation. The effects of the generated suppressor activities upon phytohemagglutinin-induced proliferation of fresh, autologous lymphocytes were measured. All three treatments resulted in significant suppression. There was no over-all difference in suppression between atopic and control groups. However, grass antigen exposure enhanced suppression by cells from atopic subjects (p. 05) but only to levels seen in concanavalin A treated cells from the same individuals. Further, the grass antigen preparation appeared to act in a non-specific fashion, resulting in similar mitogenic responses in cells from atopic and control groups. These findings bring into question the role of non-specific suppressor cells, as currently measured, in the pathogenesis of atopic disease. Allergy immunotherapy with crude antigen preparations likely results in non-specific immunologic perturbations which may enhance or depress its clinically valuable, antigen-specific, effects.
抑制细胞功能障碍被认为是人类特应性疾病中IgE反应增强的一个原因，并且变应原免疫疗法已被证明与抗原特异性抑制细胞的产生有关。为了模拟免疫疗法，对非对照受试者进行草抗原暴露的体外效应研究，采用预孵育、伴刀豆球蛋白A或不同浓度的粗制草抗原制剂进行处理。测定所产生的抑制活性对植物血凝素诱导的新鲜自体淋巴细胞增殖的影响。所有三种处理均导致显著抑制。特应性组和对照组之间在抑制方面没有总体差异。然而，草抗原暴露增强了特应性受试者细胞的抑制作用（p<0.05），但仅达到在同一受试者的伴刀豆球蛋白A处理细胞中所见的水平。此外，草抗原制剂似乎以非特异性方式起作用，导致特应性组和对照组细胞中类似的促有丝分裂反应。这些发现对目前所测定的非特异性抑制细胞在特应性疾病发病机制中的作用提出了质疑。用粗制抗原制剂进行变应原免疫疗法可能会导致非特异性免疫干扰，这可能会增强或削弱其临床上有价值的抗原特异性效应。
