Mechanisms of Neonatal Mucosal Antibody Protection

Abstract

Following an abrupt transition at birth from the sterile uterus to an environment with abundant commensal and pathogenic microbes, neonatal mammals are protected by maternal Abs at mucosal surfaces. We show in mice that different Ab isotypes work in distinct ways to protect the neonatal mucosal surface. Secretory IgA acts to limit penetration of commensal intestinal bacteria through the neonatal intestinal epithelium: an apparently primitive process that does not require diversification of the primary natural Ab repertoire. In contrast, neonatal protection against the exclusively luminal parasite Heligmosomoides polygyrus required IgG from primed females. This immune IgG could either be delivered directly in milk or retrotransported via neonatal Fc receptor from the neonatal serum into the intestinal lumen to exert its protective effect.

Autism: Maternally derived antibodies specific for fetal brain proteins

“…The transplacental passage of maternal IgG isotype antibodies has long been known as a mechanism for fetal immune instruction (Garty et al, 1994) and protection (Harris et al, 2006;Simister, 2003). A recently described organelle in the placental epithelium that expresses the low affinity IgG receptor, FcγRIIb, as well as the IgG receptor and transport protein FcRn, appears to provide a dedicated transport mechanism for maternal IgG to enter fetal circulation (Mishima et al, 2006).…”

Recognition of Gram-positive Intestinal Bacteria by Hybridoma- and Colostrum-derived Secretory Immunoglobulin A Is Mediated by Carbohydrates

“…This was illustrated in neonatal mice in which antibody immunity fixed to the hapten nitrophenol protected against bacterial challenge (47). Recently, the assessment of the crystal structure of a mucus-binding protein present at the surface of the commensal strain Lactobacillus reuteri identified motifs with potential immunoglobulin binding activity (48).…”

Immunity to gastrointestinal nematode infections

“…157 However, adoptive transfer of B cells alone from previously infected mice is insufficient to confer resistance to T. muris infection, 158 whereas transfer of IgA 159 or IgG1 (refs. 160,161) antibodies from resistant mice confers partial resistance to various nematodes, most likely because of their neutralizing effect on secreted parasite antigens, or by trapping larvae. [162][163][164][165] Given that adoptive transfer of helper T cells from previously infected mice to lymphopenic mice can confer resistance, these findings suggest that B cells might play a role in promoting the generation and/or polarization of the T-cell response, either by cytokine secretion or antigen presentation 166,167 rather than directly affecting worm expulsion.…”