Strannegård I L, Strannegård O
Acta Derm Venereol Suppl (Stockh). 1981;95:20-4.
Recent studies have given ample evidence that atopy is associated with a T-cell deficiency. This deficiency appears to be primary and not merely a consequence of disease manifestations. Several studies have indicated that the T-cell defect displays a certain selectivity, resulting in imbalance between helper and suppressor T-cell in atopics. Suppressor cells, carrying Fc IgG marker (T gamma cells) or being inducible by concanavalin A, have been found to be deficient, and recent data suggest that there is an imbalance between T8+ (cytotoxic/suppressor) and T4+ (inducer/helper) T-cells in individuals with severe atopic disease. There appears to be a negative correlation between suppressor cell activity and serum IgE levels. These findings suggest that there is a causal relationship between the T-cell deficiency and hyperproduction of IgE in atopy. The immunological abnormalities in atopy cannot be easily explained by the beta-adrenergic blockade which is associated with the disease. Further immunopharmacological studies may help to elucidate the pathogenesis of atopic disease.
最近的研究提供了充分的证据表明特应性与T细胞缺陷有关。这种缺陷似乎是原发性的,而不仅仅是疾病表现的结果。几项研究表明,T细胞缺陷表现出一定的选择性,导致特应性个体中辅助性T细胞和抑制性T细胞之间的失衡。已发现携带Fc IgG标记的抑制细胞(Tγ细胞)或可被刀豆球蛋白A诱导的抑制细胞存在缺陷,并且最近的数据表明,患有严重特应性疾病的个体中T8 +(细胞毒性/抑制性)和T4 +(诱导性/辅助性)T细胞之间存在失衡。抑制细胞活性与血清IgE水平之间似乎存在负相关。这些发现表明,T细胞缺陷与特应性中IgE的过度产生之间存在因果关系。特应性中的免疫异常不能轻易地用与该疾病相关的β-肾上腺素能阻断来解释。进一步的免疫药理学研究可能有助于阐明特应性疾病的发病机制。