Strannegård I L, Strannegård O
Int Arch Allergy Appl Immunol. 1979;58(2):167-74. doi: 10.1159/000232189.
The effect of cholera toxin and dibutyryl cAMP on mitogen-activated lymphocytes from atopic and non-atopic individuals was studied. Cholera toxin enhanced stimulation by phytohemagglutinin of cells from small children but not from adults. Dibutyryl cAMP at low concentration (less than 10(-5) M) significantly enhanced the lymphocyte response to mitogens in some, but not all individuals. High concentrations, on the other hand, were consistently inhibitory. In atopic children, the lymphocyte response to T cell mitogen was significantly less stimulated by cholera toxin, and more inhibited by dibutyryl cAMP than the response of cells from non-atopic matched controls. Thus, T cells from atopic individuals appear to have an altered sensitivity to the action of cAMP, possibly resulting in an impaired balance between helper and suppressor T cells. The hypothesis is advanced, that such an altered balance is causally related to hyperproduction of IgE resulting in atopic disease.
研究了霍乱毒素和二丁酰环磷腺苷(dibutyryl cAMP)对特应性个体和非特应性个体的丝裂原激活淋巴细胞的影响。霍乱毒素增强了植物血凝素对幼儿细胞的刺激作用,但对成人细胞无此作用。低浓度(小于10^(-5) M)的二丁酰环磷腺苷在一些但并非所有个体中显著增强了淋巴细胞对丝裂原的反应。另一方面,高浓度则始终具有抑制作用。在特应性儿童中,与非特应性匹配对照的细胞反应相比,霍乱毒素对T细胞丝裂原的淋巴细胞反应刺激明显较弱,而二丁酰环磷腺苷的抑制作用更强。因此,特应性个体的T细胞似乎对环磷腺苷的作用敏感性发生了改变,这可能导致辅助性T细胞和抑制性T细胞之间的平衡受损。有人提出这样一种假说,即这种平衡改变与导致特应性疾病的IgE过度产生存在因果关系。