Abstract

Since placenta of pregnant sows are impermeable to immunoglobulin passage, the neonates are born agammaglobulinemic; although immunocompetent, they are unable to develop rapidly an immune response which will protect their systemic and mucosal compartments; thus their survival depend upon the passive acquisition of maternal immunity including at least 3 components: i) a systemic humoral immunity, transmitted through colostrum conveying mainly by IgG; these IgG are transferred from maternal serum via Fc gamma receptors on the epithelial cells of mammary gland (MG). ii) a local humoral immunity, especially secretory IgA (IgAs), transmitted mainly by milk (lactogenic immunity) until weaning. IgAs are secreted by MG recruited plasma cells and are excreted in milk via secretory component of epithelial cells: these IgA exhibit a specificity for the antigens present in the maternal digestive tract, the so-called "entero-mammary link"; this link is due to the migration of lymphocytes from the gut to the mammary gland; they are recruited from the blood via the interaction of their homing receptor (alpha 4 beta 7) with the developmentally regulated mucosal vascular addresin MadCAM-1. In the MG, MadCAM-1 increased in pregnancy (probably under oestrogenic stimulation) but regressed in lactation; its density is closely related to the T cell numbers in MG; in contrast the increase in plasma cell numbers is not related to MadCAM-1 density. Thus IgA precursor cells (alpha 4 beta 7 B cells) seem to be recruited by a milk B cell chemoattractant. On the other hand, presence of T and B lymphocytes in MG (some of them originating from the systemic compartment), sustains the attempts of MG immunization and the results sustain the view of a true local immune response. iii) possibly but not formally proved, a cellular immunity transmitted via maternal immunocompetent cells present in mammary secretions; the exported lymphocytes may represent a selected population of lymphocytes after their passage through the MG epithelium.

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