B lymphocyte development in fetal liver

Abstract

AbstractSingle cell suspensions of fetal liver cells, prepared from embryos at day 13 of gestation until birth, develop mitogen bacterial lipopolysaccharide (LPS)‐reactive B cells “in vitro” within the same time as they do “in vivo”. The development of these mitogen LPS‐reactive B cells in vitro is dependent on unknown components of fetal calf serum, found in some but not all batches. It does not require the presence of the corresponding B cell mitogens, i.e. LPS, in culture. Fetal liver cells, put in culture at different times of gestation, all acquire LPS reactivity at the equivalent of birth in vitro. When the cells have become LPS‐reactive, they are then stimulated by LPS to growth and maturation into clones of IgM‐secreting, IgA‐secreting and IgG‐secreting plaque‐forming cells (PFC). The development of these PFC responses is mitogen‐dependent: in the absence of LPS only 2‐5 % of the LPS‐stimulated PFC responses develop. Only the magnitude, but not the development in time, of LPS reactivity of fetal liver cells is different in vivo and in vitro. This may indicate either that an early precursor cell to LPS‐reactive B cells can only divide in vivo but not in vitro, or that early precursors continue to migrate with time of gestation into fetal liver. After birth B cells in liver are immediately reactive to LPS; however, they rapidly leave the liver.Few, if any, dextrans sulfate or lipoprotein‐reactive B cells, yielding a PFC response, develop in fetal liver cells either in vivo or in vitro. Neonatal spleen contains immediately mitogen‐reactive B cells. Comparable numbers of LPS, dextran sulfate and lipoprotein‐reactive cells are found.Development of fetal liver cells to Ig‐secreting PFC, occurs, therefore, in two stages. The first (pre‐B → B) is independent of externally added mitogen (such as LPS), the second (B → PFC) requires the addition of mitogen. The majority of spleen cells have already passed this first stage of development.