Rosenberg Y J
J Exp Med. 1979 Dec 1;150(6):1561-6. doi: 10.1084/jem.150.6.1561.
Normal mice spontaneously develop plaque-forming cells (PFC) specific for antigens on modified self erythrocytes (bromelain-treated mouse erythrocytes [BrMRBC] antigens). Our study demonstrates that the sex-linked defect that results in the inability of CBA/N mice to respond to several T-independent antigens (TI-2 antigens) also regulates the autoantibody response to BrMRBC antigens. Thus, in CBA/N homozygous mice and male F1 offspring of CBA/N-mothered crosses, e.g., (CBA/N X NZB)F1 males, such PFC are absent. To examine whether specific autoreactive B cells are present in defective mice, the latter were stimulated either nonspecifically with the mitogen LPS or by infection with lethal malaria (17XL Plasmodium yoelii) known to induce anti-BrMRBC PFC specifically. The results indicate that modest antibody responses to self antigens could be induced in young (5- to 7-wk old) defective mice and that these responses increased as a function of age. The data is consistent with the view that the defect in CBA/N mice does not result from an absence of functional anti-BrMRBC B cells but rather from low frequencies of the specific precursors, which can be triggered and expanded with age probably by environmental stimulations.
正常小鼠会自发产生针对修饰自身红细胞（菠萝蛋白酶处理的小鼠红细胞[BrMRBC]抗原）上抗原的斑块形成细胞（PFC）。我们的研究表明，导致CBA/N小鼠无法对几种T细胞非依赖性抗原（TI-2抗原）作出反应的性连锁缺陷，也调节了对BrMRBC抗原的自身抗体反应。因此，在CBA/N纯合小鼠以及CBA/N作为母本杂交的雄性F1后代中，例如（CBA/N×NZB）F1雄性小鼠，不存在此类PFC。为了检查缺陷小鼠中是否存在特异性自身反应性B细胞，用丝裂原LPS对缺陷小鼠进行非特异性刺激，或用已知能特异性诱导抗BrMRBC PFC的致死性疟疾（17XL约氏疟原虫）感染缺陷小鼠。结果表明，在年轻（5至7周龄）的缺陷小鼠中可诱导出对自身抗原的适度抗体反应，且这些反应随年龄增长而增强。数据与以下观点一致：CBA/N小鼠的缺陷并非源于功能性抗BrMRBC B细胞的缺失，而是源于特异性前体细胞的低频率，这些前体细胞可能随年龄增长受到环境刺激而被触发并扩增。
