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Human B lymphocytes are inherently immature at birth (Holladay and Smia-lowicz 2000). Despite significant production of IgM and IgG immunoglobulin in the fetus, production of these immunoglobulin isotypes at birth is impaired (Holt and Jones 2000). Neonates have very low levels of serum IgM, IgA, and IgE, and essentially all IgG is of maternal origin (Holladay and Smialowicz 2000; Holt and Jones 2000). IgM synthesis is reported to begin during the first week of extrauterine life regardless of the gestational age at birth (Vetro and Bellanti 1989). IgM levels rapidly reach 50% of the adult values by 6 months and 75 to 80% of the adult levels by 1 year of age (de Muralt 1978). IgA synthesis results in only 20% of the adult level by 12 months of age; adult levels are not reached until 10 years of age (de Muralt 1978; Vetro and Bellanti 1989). Maternally derived newborn IgG decreases to a low at 3 months of age, then synthesis by the newborn begins and adult levels are reached by 5 to 6 years of age (Holladay and Smialowicz 2000). The low IgE levels are the consequence of a lack of IL-4 produced by immature helper T cells and reduced CD40L expression on these T cells (Holt and Jones 2000). Approximately three-quarters of B cells in the neonate express the CD5 cell surface marker, whereas only approximately one-quarter of the B cells express this marker in adult cells (Hannet et al. 1992). It has been hypothesized that because CD5+ B cells produce polyreactive antibody and are largely T-independent (Peak-man et al. 1992), these cells may play a vital role in the infant's primary immune response (Holt and Jones 2000). Despite the presence of this type of B cell, the neonate's inability to respond to polysaccharide vaccines such as Haemophilus influenzae type b (Hib) (Ahmad and Chapnick 1999; Cadoz, 1998; Gathings et al. 1981) has revealed a weakness in the defense system of the infant that lasts until 1 to 2 years of age (Ahmad and Chapnick 1999; Cadoz 1998; Rijkers et al. 1998; West 2002). Polysaccharides activate B cells through a required costimulation of surface immunoglobulin and CD21, type 2 complement receptor. Reduced CD21 in neonates may explain their unresponsiveness to polysaccharides (Rijkers et al. 1998). The delays in B lymphocyte function have been attributed to a variety of different causes: deficiency in B cells (Anderson et al. 1981; Gathings et al. 1981), regulation by T suppressor cells (Miyawaki et al. 1981), and defects in accessory cell function (Bondada et al. 2000).

Similar to the requirement of antigenic exposure for maturation of the T cell compartment, B lymphocytes appear to be influenced by antigenic exposure in utero and during early postnatal life. Evidence from laboratory studies demonstrates that animals raised in germ-free environments have delayed lymphoid development (Thorbecke 1959). Moreover, a significant body of research addresses maternal influences on the baby during pregnancy (due to diet [Bjorksten1999a; Moore 1998], illness [Goldman and Marchant 2003; Zinkernagel 2003], allergens [Warner and Warner 2000], or vaccines [Glezen and Alpers 1999]) and after parturition (through breastfeeding [Bjorksten 1999b; Hanson 1998; Oddy 2002]), indicating that exposure to antigens through the mother can aid or impair maturation of the infant's immune system.

Finally, exposure of the infant to microorganisms, especially those of the gut, and to vaccines enhances serum immunoglobulin titers (de Muralt 1978). The response to encapsulated gut flora (particularly strains of Escherichia coli) (Fong et al. 1974) drives development of IgM isohemagglutinins that recognize the ABO blood group antigens. Clinically, a window of opportunity exists because the response to carbohydrates does not develop for 6 months or more (Fong et al. 1974). Heart transplantation in infants has now been successfully used despite ABO incompatibility of the donor and recipients (West et al. 2001).

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