Bcell homing to mammary glands

Lactating mammary glands are part of the integrated mucosal immune system, and milk antibodies reflect antigenic stimulation of MALT in the gut as well as in the airways. This fact has been documented by showing that SIgA from breast milk exhibits antibody specificities for an array of common intestinal and respiratory pathogens (Goldman, 1993). The secretory antibodies are thus highly targeted against infectious agents in the mother's environment, which are those likely to be encountered by the infant during its first weeks of life. Therefore, breast-feeding represents an ingenious immunological integration of mother and child (Fig. 14.4). Although the protection provided by this humoral defence mechanism is most readily demonstrable in populations living in poor sanitary conditions (Hanson et al., 1993; Anon., 1994), a beneficial clinical effect is also apparent in the industrialized world (Wold and Hanson, 1994),

  1. 14.4. Integration of mucosal immunity between mother and the newborn. The figure emphasizes migration (arrows) of primed B- (and probably T-) cells from gut-associated lymphoid tissue (GALT), such as Peyer's patches, via lymph and peripheral blood to lactating mammary glands. This distribution of precursors for immunoglobulin (lg)A plasma cells beyond the gut mucosa is crucial for glandular production and subsequent occurrence in breast milk of secretory antibodies (SlgA and SlgM) specific for enteric antigens (microorganisms and food proteins). By this mechanism, the breast-fed infant will receive relevant secretory antibodies directed against the microflora initially colonizing its mucosae (reflecting the mother's microflora) and hence be better protected both in the gut and in the upper airways by SlgA and SlgM (hatched areas), in the same way as the mother's gut mucosa is protected by similar antibodies (hatched areas).
  2. 14.4. Integration of mucosal immunity between mother and the newborn. The figure emphasizes migration (arrows) of primed B- (and probably T-) cells from gut-associated lymphoid tissue (GALT), such as Peyer's patches, via lymph and peripheral blood to lactating mammary glands. This distribution of precursors for immunoglobulin (lg)A plasma cells beyond the gut mucosa is crucial for glandular production and subsequent occurrence in breast milk of secretory antibodies (SlgA and SlgM) specific for enteric antigens (microorganisms and food proteins). By this mechanism, the breast-fed infant will receive relevant secretory antibodies directed against the microflora initially colonizing its mucosae (reflecting the mother's microflora) and hence be better protected both in the gut and in the upper airways by SlgA and SlgM (hatched areas), in the same way as the mother's gut mucosa is protected by similar antibodies (hatched areas).

even in relation to relatively common diseases, such as otitis media and acute lower respiratory tract infections (Pisacane et al., 1994; Newman, 1995; Golding et al., 1997).

Antibodies to various dietary antigens, such as cow's milk proteins (Savilahti et al., 1991) and gluten (Juto and Holm, 1992), are also present in breast milk. However, little is known about the preferential site where soluble luminal antigens exert immune priming. Thus, dietary proteins may be taken up mainly through the extensive epithelial surfaces covering the diffuse immunological effector tissue of the intestinal mucosa rather than by M cells, and may therefore be largely transported to the mesenteric lymph nodes. As discussed below, their fate and possible immune-inductive or tolerogenic effects will depend on how they are handled locally and whether they reach lymph or portal blood (Brandtzaeg et al., 1987; Sanderson and Walker, 1993; Brandtzaeg, 1996a).

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