Wands J R, Dienstag J L, Weake J R, Koff R S
Clin Exp Immunol. 1981 May;44(2):396-404.
Elevated serum immunoglobulin levels are a frequent finding in patients with severe alcoholic liver disease. We measured in vitro peripheral blood lymphocyte IgA synthesis by radioimmunoassay in 13 patients with severe alcoholic liver disease and hypergammaglobulinaemia and in normal control subjects. We found an increase in spontaneous IgA synthesis compared to controls (P greater than 0.001). On the other hand, there was no difference between groups in percentage stimulation of IgG production by B cells exposed to pokeweed mitogen. We also searched for defects in concanavalin A (Con A) induced suppressor T cell activity. There was no difference between patients with alcoholic liver disease and controls in the capability of such suppressor T cells to inhibit the response of allogeneic cells to a T cell mitogen. Similarly, we examined the capability of Con A-induced suppressor T cells to inhibit pokeweed mitogen-stimulated IgG synthesis by both autologous and allogeneic responder cells and observed no difference between alcoholic patients and controls. Thus these measured suppressor T-T and T-B cell interactions appeared no different from those in control subjects. Our studies suggest, therefore, that B cell IgG synthesis in vitro is enhanced in alcoholic liver disease. Furthermore, the capability to induce suppressor T cells which affects both T and B cell function appears intact; a finding in contrast to our previous observation in chronic active hepatitis. The investigations suggest that enhanced spontaneous IgG synthesis in vitro may result from intense antigenic stimulation in vivo.
血清免疫球蛋白水平升高在重症酒精性肝病患者中很常见。我们用放射免疫分析法测定了13例重症酒精性肝病伴高球蛋白血症患者及正常对照者外周血淋巴细胞体外IgA合成情况。我们发现与对照组相比,自发性IgA合成增加(P大于0.001)。另一方面,暴露于商陆有丝分裂原的B细胞对IgG产生的刺激百分比在两组之间没有差异。我们还研究了伴刀豆球蛋白A(Con A)诱导的抑制性T细胞活性缺陷。酒精性肝病患者与对照组在这类抑制性T细胞抑制同种异体细胞对T细胞有丝分裂原反应的能力方面没有差异。同样,我们检测了Con A诱导的抑制性T细胞抑制自体和同种异体反应细胞受商陆有丝分裂原刺激的IgG合成的能力,发现酒精性肝病患者与对照组之间没有差异。因此,这些检测到的抑制性T-T和T-B细胞相互作用似乎与对照组无差异。因此,我们的研究表明,酒精性肝病患者体外B细胞IgG合成增强。此外,诱导影响T和B细胞功能的抑制性T细胞的能力似乎完好无损;这一发现与我们之前在慢性活动性肝炎中的观察结果相反。这些研究表明,体外自发性IgG合成增强可能是由于体内强烈的抗原刺激所致。