Analysis of Clonable Cells in Embryonic Liver Suspensions

New Zealand Black (NZB) mice have long been exploited as a model of genetically controlled autoimmune diseases and immunoregulatory dysfunction (1-3). Of particular concern to us is the unusual development and function of their humoral immune system. There is reason to believe that spontaneous and polyclonal activation of B cells occurs independently of defects residing in thymus-derived (T) cells (2-4). For example, this occurs in cell transfer situations and in mutant athymic mice with the NZB background (5-6). In discerning which of the abnormal features of these animals are intrinsic and which represent changes that occur secondarily to defects in other systems, it is helpful to establish the chronology of events during ontogeny. Previous reports (7-9) indicated that NZB mice may become immunologically mature at an early age and that hypersecreting B lineage cells were detectable even from the time of birth. The present study, using a mitogen-dependent colony-forming cell assay, reveals that abnormalities affecting development of the humoral immune system occur much earlier in embryos of this interesting strain of mice.