Mechanisms of acquired response in oral cavity

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Mechanisms of acquired response in oral cavity

  • In general, the reactions of acquired (adaptive) immunity are much more complex and intricate affecting all lineages of immune cells. In oral cavity antigen-specific immune response originates from two main sources.
  • First, oral pathogens trigger direct activation of resident immune cells of salivary glands. Among them are antigen-presenting cells (APC), consisting of dendritic cells (DC), macrophages, and B lymphocytes. Microbial antigens undergo natural retrograde flow along the salivary ducts. Next, they are delivered to immune cells via endocytosis by ductal epithelium.
  • Second, specific immune response in the oral cavity is maintained by continuous migration of Ag-specific immune cells to salivary glands from primary sites of antigenic exposure, mainly from gut-associated lymphoid tissues or GALT.
  • These cells comprise activated T lymphocytes and specific B cells capable of IgA synthesis. The lymphoid follicles of GALT carry follicle-associated epithelial cells (FAE cells) or microfold cells (M cells) that capture and transport exogenous antigens from the lumen of the small intestine to neighbouring dendritic cells for antigen presentation. Afterwards, antigen-stimulated immune cells begin to spread to various peripheral sites of the immune system including the oral cavity.
  • Similar with GALT, expansion of primed immunocompetent cells to oral cavity occurs from NALT, or nasal mucosa-associated lymphoid tissues (tonsils and other accumulations of lymphoid follicles within Waldeyer’s pharyngeal lymphatic ring).
  • Taken together, it can be concluded that IgA-producing plasma cells and effector T lymphocytes of oral cavity originate from a common mucosal immune system. The latter is the sum of local mucosal lymphoid tissues present in peripheral body compartments and organs.
  • Specific acquired response against thymus-dependent Ags initiates multiple immune reactions that profoundly affect the host immunity.
  • The principal event that biases the immune reactivity towards cellular inflammatory response is the transformation of naive Th0 cells into Th1 cell type, whereas conversion of Th0 lymphocytes into Th2 cells activates humoral response and antibody production.
  • Th1 and Th2 are characterized by the opposite type of cytokine secretion. The basic cytokines, produced by Th1 cells are γ-interferon, IL-2 and β-TNF, whereas cytokines of Th2 encompasses IL-4, IL-5, IL-6, IL-10, IL-13, and some others. Th1/Th2 activity re-directs next immune reactions into a cell-mediated inflammatory response or towards B cell stimulation and antibody synthesis (humoral response).
  • Multiple effector mechanisms ensuring the elimination of invaded pathogen include cell recruitment to inflammatory focus, stimulation of phagocytosis and antigenic presentation, cytotoxic action of T killers and NK cells, conversion of B cells into plasma cells with the secretion of antibodies of various Ig classes.

References

  1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4170154/
  2. https://www.researchgate.net/publication/264629535_The_mucosal_immune_system_in_the_oral_cavity-an_orchestra_of_T_cell_diversity