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Cell Rep ; 18(2): 419-431, 2017 01 10.
Article in English | MEDLINE | ID: mdl-28076786

ABSTRACT

Whereas type I interferons (IFNs-I) were proposed to be elevated in human periodontitis, their role in the disease remains elusive. Using a bacterial-induced model of murine periodontitis, we revealed a prolonged elevation in IFN-I expression. This was due to the downregulation of TAM signaling, a major negative regulator of IFN-I. Further examination revealed that the expression of certain TAM components was reduced as a result of prolonged degradation of MYD88 by the infection. As a result of such prolonged IFN-I production, innate immunological functions of the gingiva were disrupted, and CD4+ T cells were constitutively primed by dendritic cells, leading to elevated RANKL expression and, subsequently, alveolar bone loss (ABL). Blocking IFN-I signaling restored proper immunological function and prevented ABL. Importantly, a loss of negative regulation on IFN-I expression by TAM signaling was also evident in periodontitis patients. These findings thus suggest a role for IFN-I in the pathogenesis of periodontitis.


Subject(s)
Interferon Type I/biosynthesis , Myeloid Differentiation Factor 88/metabolism , Porphyromonas gingivalis/physiology , Proteolysis , Receptors, Cell Surface/metabolism , Signal Transduction , Alveolar Bone Loss/complications , Alveolar Bone Loss/immunology , Alveolar Bone Loss/pathology , Animals , Bacteroidaceae Infections/complications , Bacteroidaceae Infections/immunology , Bacteroidaceae Infections/microbiology , Bone Resorption/complications , Bone Resorption/immunology , Bone Resorption/pathology , Dendritic Cells/immunology , Gingiva/microbiology , Gingiva/pathology , Humans , Interferon Type I/metabolism , Leukocytes/pathology , Lymph Nodes/pathology , Mice , Mouth Mucosa/microbiology , Mouth Mucosa/pathology , Periodontitis/immunology , Periodontitis/microbiology , Periodontitis/pathology
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