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Brandtzaeg, P. (2013). Secretory immunity with special reference to the oral cavity. Journal of Oral Microbiology, 5(1), 20401. Added by: Dr. Enrique Feoli (29/09/2020, 16:32) Last edited by: Dr. Enrique Feoli (03/01/2026, 16:46) |
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| Resource type: Journal Article DOI: 10.3402/jom.v5i0.20401 BibTeX citation key: Brandtzaeg2013 View all bibliographic details  |
Categories: BioAcyl Corp Subcategories: Inmunidad de mucosas Creators: Brandtzaeg Collection: Journal of Oral Microbiology |
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| Abstract |
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The two principal antibody classes present in saliva are secretory IgA (SIgA) and IgG; the former is produced as dimeric IgA by local plasma cells (PCs) in the stroma of salivary glands and is transported through secretory epithelia by the polymeric Ig receptor (pIgR), also named membrane secretory component (SC). Most IgG in saliva is derived from the blood circulation by passive leakage mainly via gingival crevicular epithelium, although some may be locally produced in the gingiva or salivary glands. Gut-associated lymphoid tissue (GALT) and nasopharynx-associated lymphoid tissue (NALT) do not contribute equally to the pool of memory/effector B cells differentiating to mucosal PCs throughout the body. Thus, enteric immunostimulation may not be the best way to activate the production of salivary IgA antibodies although the level of specific SIgA in saliva may still reflect an intestinal immune response after enteric immunization. It remains unknown whether the IgA response in submandibular/sublingual glands is better related to B-cell induction in GALT than the parotid response. Such disparity is suggested by the levels of IgA in submandibular secretions of AIDS patients, paralleling their highly upregulated intestinal IgA system, while the parotid IgA level is decreased. Parotid SIgA could more consistently be linked to immune induction in palatine tonsils/adenoids (human NALT) and cervical lymph nodes, as supported by the homing molecule profile observed after immune induction at these sites. Several other variables influence the levels of antibodies in salivary secretions. These include difficulties with reproducibility and standardization of immunoassays, the impact of flow rate, acute or chronic stress, protein loss during sample handling, and uncontrolled admixture of serum-derived IgG and monomeric IgA. Despite these problems, saliva is an easily accessible biological fluid with interesting scientific and clinical potentials.
Added by: Dr. Enrique Feoli Last edited by: Dr. Enrique Feoli |
| Notes |
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In line with the latter observation, at least one fourth of IgA+ PCs in human ileal lamina propria have been shown to produce polyreactive antibodies, which nevertheless were found to be somatically mutated with signs of antigen-driven selection (Citation139). Other studies have shown that IgA autoantibodies produced in human duodenal mucosa are of high affinity but with little adaptation by somatic mutations, exhibiting mainly a germline repertoire (Citation140). Notably in this context, recent mouse experiments suggested that there may be two fundamentally differentiation pathways for memory B cells – one dedicated to generation of high-affinity somatic antibody mutants, while the other preserves antibody germline specificities to arm the host for rapid responses to encountered variants of potentially dangerous antigens (Citation141) – perhaps including the commensal microbiota. The latter immunological feature is characteristic for the IgA repertoire of human neonates (Citation142), as also reflected in neonatal saliva (Citation143). This situation is followed postnatally by a slow immune maturation with the somatic mutation frequency of IgA VH-gene transcripts reaching 25% of adult levels at the age of approximately 5 months (Citation142). In fact, both the duodenal and the parotid frequency of IgA VH mutations of adults is much higher than that in the adult human spleen, probably reflecting the constant antigenic pressure on the mucosal immune system (Citation144). In the laboratory rat, however, a more restricted IgA repertoire (near germline) was revealed in salivary glands than in the distal small intestine (Citation145).
Other recent mouse experiments demonstrated that the commensal coating with IgA in feces depends on appropriate clonal B-cell selection and affinity maturation in GALT germinal centers, and perhaps to some extent also in the lamina propria (Citation146). In human feces some 40% of the anaerobic bacteria are normally coated with IgA (Citation147) and this phenomenon can be observed in early childhood (Citation148). Such IgA containment is probably important for the mutual host–microbe interaction, contributing to sustainable homeostasis by dampening proinflammatory signaling in the host and providing an immune pressure on commensal bacteria which results in antigenic drift without dysbiosis (Citation146, Citation149). Altogether, however, it has to be admitted that many open questions remain about the mucosal IgA responses, both in mice and humans (Citation150). Added by: Dr. Enrique Feoli Last edited by: Dr. Enrique Feoli |