Oliveira G G, Hutchings P R, Roitt I M, Lydyard P M
Department of Immunology, University Collge London Medical School, UK.
Clin Exp Immunol. 1994 May;96(2):297-302. doi: 10.1111/j.1365-2249.1994.tb06557.x.
NZB mice spontaneously develop haemolytic anaemia as the result of production of erythrocyte autoantibodies. The mechanisms leading to breakdown in tolerance to erythrocyte autoantigens are unknown. Antibodies to CD4 have been successfully used to treat several murine models of autoimmune disease. In this study we injected NZB mice with non-depleting CD4 antibodies and were able to prevent and abrogate erythrocyte autoantibody production in young (Coombs' negative) and old (Coombs' positive) mice, respectively. Our data indicate the dependency of autoantibody production on CD4+ T cells. However, withdrawal of anti-CD4 antibodies resulted in the appearance of erythrocyte autoantibodies, showing that under these conditions we were unable to re-establish tolerance to autoantigens on erythrocytes using anti-CD4 treatment.
NZB小鼠由于产生红细胞自身抗体而自发发展为溶血性贫血。导致对红细胞自身抗原耐受性破坏的机制尚不清楚。抗CD4抗体已成功用于治疗多种自身免疫性疾病的小鼠模型。在本研究中,我们给NZB小鼠注射非耗竭性CD4抗体,分别能够预防和消除年轻(库姆斯试验阴性)和年老(库姆斯试验阳性)小鼠的红细胞自身抗体产生。我们的数据表明自身抗体产生对CD4+T细胞的依赖性。然而,停用抗CD4抗体导致红细胞自身抗体出现,表明在这些条件下,我们无法使用抗CD4治疗重新建立对红细胞自身抗原的耐受性。