Dendritic cells: microbial clearance via autophagy and potential immunobiological consequences for periodontal disease
Identifieur interne : 000E48 ( Main/Exploration ); précédent : 000E47; suivant : 000E49Dendritic cells: microbial clearance via autophagy and potential immunobiological consequences for periodontal disease
Auteurs : Ahmed R. El-Awady ; Roger M. Arce ; Christopher W. CutlerSource :
- Periodontology 2000 [ 0906-6713 ] ; 2015-10.
Abstract
Dendritic cells are potent antigen‐capture and antigen‐presenting cells that play a key role in the initiation and regulation of the adaptive immune response. This process of immune homeostasis, as maintained by dendritic cells, is susceptible to dysregulation by certain pathogens during chronic infections. Such dysregulation may lead to disease perpetuation with potentially severe systemic consequences. Here we discuss in detail how intracellular pathogens exploit dendritic cells and escape degradation by altering or evading autophagy. This novel mechanism explains, in part, the chronic, persistent nature observed in several immuno‐inflammatory diseases, including periodontal disease. We also propose a hypothetical model of the plausible role of autophagy in the context of periodontal disease. Promotion of autophagy may open new therapeutic strategies in the search of a ‘cure’ for periodontal disease in humans.
Url:
- https://api.istex.fr/ark:/67375/WNG-4Z389DK4-T/fulltext.pdf
- http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4530502
DOI: 10.1111/prd.12096
Affiliations:
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<front><div type="abstract">Dendritic cells are potent antigen‐capture and antigen‐presenting cells that play a key role in the initiation and regulation of the adaptive immune response. This process of immune homeostasis, as maintained by dendritic cells, is susceptible to dysregulation by certain pathogens during chronic infections. Such dysregulation may lead to disease perpetuation with potentially severe systemic consequences. Here we discuss in detail how intracellular pathogens exploit dendritic cells and escape degradation by altering or evading autophagy. This novel mechanism explains, in part, the chronic, persistent nature observed in several immuno‐inflammatory diseases, including periodontal disease. We also propose a hypothetical model of the plausible role of autophagy in the context of periodontal disease. Promotion of autophagy may open new therapeutic strategies in the search of a ‘cure’ for periodontal disease in humans.</div>
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