Abstract
The major mechanisms of mucosal defense in the neonate consist of a variety of nonspecific barriers, and innate and specific adaptive immune responses. The functions of innate immunity in the mucosal surfaces are mediated by host-specific microbial–pathogen recognition receptors, designed to recognize unique microbial-associated molecular patterns integral to the structure of most microorganisms. Other mechanisms include many antimicrobial peptides, macrophages, dendritic cells, complement components and host-derived cellular and soluble products. The important elements of neonatal mucosal adaptive immunity include the inductive sites, such as the Peyer‘s patches and other lymphoid structures in the respiratory and gastrointestinal tracts, the nasopharyngeal and sublingual tissues, the subepithelial and intraepithelial sites in most external mucosal surfaces, including the genital tract and the mammary glands. These sites contain lymphoid cells derived by the homing of antigen-activated cells from the inductive sites. Activated B cells, mostly IgA (up to 80%) are detected in the mucosal tissues shortly after birth. However, IgA-producing plasma cells are generally detected in the mucosa approximately 7–10 days of age. With progressive environmental antigenic stimulation, the number of circulating IgA cells increase significantly by 1 month of age. The postnatal development of mucosal immunity is critically influenced by the acquisition and nature of mucosal microflora, and the temporal nature and qualitative and quantitative aspects of dietary antigens and other environmental agents introduced in the neonatal period. Mucosal immune responses are generally protective against disease-producing organisms and environmental macromolecules. The mucosal immune responses may also be pathologic and foster the induction of immunologically mediated disease states and autoimmunity. The development of secretory IgA and other antimicrobial mucosal responses as well as the induction of tolerance in the neonatal period and early infancy are essential for the maintenance of mucosal homeostasis in early childhood and prevention of disease later in life.
Financial & competing interests disclosure
The author has no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
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