B lymphocyte development and function in the neonate

Pre-B cells express cytoplasmic p chain and lack surface immunoglobulin (Ig). In humans, pre-B cells are detected in fetal liver and omentum as early as 7-8 weeks of gestation. One to two weeks later, B lymphocytes (surface IgM+) are found in fetal liver and the development of B lymphocytes expressing other surface Ig isotypes follows. In the mouse, the earliest B lineage precursor cells can be identified as CD45R (B220)+ cells in fetal liver at -12-13 days gestation. B lineage cell development also involves the surrogate light chains, (e.g. X5, VpreB) which are expressed both in pro-B cells and, as a complex with p chain, in pre-B cells. Surrogate light chain (\5) transcription is seen by day 13 in fetal liver and pre-B cells are evident by day 14. Pre-B cells exhibit heterogeneity in surface antigen expression (e.g. CD4.3) and in expression of other molecules (e.g. RAG-1, RAG-2) indicative of their activity and precise stage of maturation. B lineage precursors from adult mice differ from those seen early in ontogeny. For example, murine fetal pre-B cells do not express major histocompatibility complex (MHC) class II antigens, in contrast to adult pre-B cells. B cells are clearly demonstrable in murine fetal liver by days 16-17 of gestation; these fetal B cells are generally restricted to expression of surface IgM. Eventually, the bone marrow becomes the main organ of B lymphopoiesis in both mouse and human throughout adult life.

IgM synthesis has been detected as early as 10-12 weeks of gestation in the human fetus; however, serum concentrations of IgM in the newborn are approximately 10% of those observed in adults and do not reach adult levels until 1-2 years of age. Serum concentrations of nonmaternal IgG are also abnormally low in the neonate and do not approach adult concentrations until 4-6 years of age.

Developmentally, immunocompetence does not extend to all antigens and, early in ontogeny, humans are constrained in their capacity to mount humoral responses to carbohydrate antigens. Children less than 2 years of age are generally deficient in response to unmodified bacterial polysaccharide vaccines. This, in turn, may contribute to the susceptibility of infants to certain bacterial infections (e.g. Streptococcus pneumoniae).

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