Krawitt E L, Kilby A E, Albertini R J, Schanfield M S, Chastenay B F, Harper P C, Mickey R M, McAuliffe T L
Department of Medicine, University of Vermont, Burlington 05405.
Clin Immunol Immunopathol. 1988 Feb;46(2):249-57. doi: 10.1016/0090-1229(88)90187-0.
Some patients with autoimmune chronic active hepatitis as well as their disease-free first degree relatives show decreased suppressor cell activity of peripheral blood T lymphocytes. Studies were therefore undertaken in families ascertained by the presence of a single chronic active hepatitis patient to determine if this abnormality of immune regulation represents a genetic phenotype simply controlled by a gene or genes at a putative disease susceptibility locus and, further, if this locus showed linkage to either the HLA or the immunoglobulin constant region loci. In addition to determining circulating autoantibody status and genotyping for HLA and immunoglobulin allotypes, suppressor T cells were evaluated by surface markers and by determining their ability to suppress IgG secretion in vitro. The results suggest that immunoregulatory dysfunction in autoimmune chronic active hepatitis is a familial abnormality, but that this abnormality occurs independent of circulating autoantibody status and of the segregation of genes for HLA or immunoglobulin allotypes.
一些自身免疫性慢性活动性肝炎患者及其无病的一级亲属外周血T淋巴细胞的抑制细胞活性降低。因此，对由单一慢性活动性肝炎患者确诊的家族进行了研究，以确定这种免疫调节异常是否代表一种简单地由一个或多个假定疾病易感位点的基因控制的遗传表型，此外，该位点是否与HLA或免疫球蛋白恒定区基因座连锁。除了确定循环自身抗体状态以及对HLA和免疫球蛋白同种异型进行基因分型外，还通过表面标志物以及确定其体外抑制IgG分泌的能力来评估抑制性T细胞。结果表明，自身免疫性慢性活动性肝炎中的免疫调节功能障碍是一种家族性异常，但这种异常的发生与循环自身抗体状态以及HLA或免疫球蛋白同种异型基因的分离无关。
