Russell P J, Cunningham J, Dunkley M, Wilkinson N M
Clin Exp Immunol. 1981 Sep;45(3):496-503.
The course of haemolytic anaemia in NZB mice has been altered by injection of spleen cells from diseased mice into younger ones before the onset of clinical disease. Recipients greater than 6 weeks of age developed early-onset autoimmune disease, recipients less than 6 weeks of age developed early-onset autoimmune disease, recipients less than 6 weeks of age recovered from early induced disease and showed a delay in the onset of spontaneous disease as compared with untreated NZB mice. This delay was due to the induction in the young mice of splenic suppressor cells. These cells were non-adherent to nylon wool and suppressed autoantibody formation on transfer to old Coombs-positive recipients. Suppressor cells active against autoantibody formation on transfer to old Coombs-positive recipients. Suppressor cells active against autoantibody-producing cells may be present in young untreated NZB mice, but not in sufficient numbers to suppress autoantibody production on adoptive transfer to Coombs-positive; however, when Ig-negative cells from the spleens of very young NZB mice were transferred together with Ig-positive cells from Coombs-positive donor mice to irradiated NZB recipients, the autoantibody production of the transferred B cells was suppressed in some cases. Suppressor cell activity could also be induced by co-culture of spleen cells from old Coombs-positive and young Coombs-negative NZB mice in vitro.
在临床疾病发作前，将患病小鼠的脾细胞注射到年幼的新西兰黑（NZB）小鼠体内，改变了NZB小鼠溶血性贫血的病程。6周龄以上的受体出现早发性自身免疫性疾病，6周龄以下的受体也出现早发性自身免疫性疾病，6周龄以下的受体从早期诱发疾病中恢复，与未治疗的NZB小鼠相比，自发性疾病的发作出现延迟。这种延迟是由于幼鼠体内诱导产生了脾抑制细胞。这些细胞不黏附于尼龙毛，转移到旧的抗人球蛋白试验（Coombs）阳性受体后可抑制自身抗体的形成。转移到旧的Coombs阳性受体后对自身抗体形成有活性的抑制细胞。对自身抗体产生细胞有活性的抑制细胞可能存在于未治疗的年幼NZB小鼠中，但数量不足以在过继转移到Coombs阳性受体时抑制自身抗体的产生；然而，当将非常年幼的NZB小鼠脾脏中的Ig阴性细胞与Coombs阳性供体小鼠的Ig阳性细胞一起转移到经辐射的NZB受体时，在某些情况下，转移的B细胞的自身抗体产生受到抑制。通过将旧的Coombs阳性和年幼的Coombs阴性NZB小鼠的脾细胞在体外共同培养，也可诱导抑制细胞活性。
