Activation of invariant NK T cells in periodontitis lesions.
Periodontitis is one of the most prevalent human inflammatory diseases. The major clinical phenotypes of this polymicrobial, biofilm-mediated disease are chronic and aggressive periodontitis, the latter being characterized by a rapid course of destruction that is generally attributed to an altered immune-inflammatory response against periodontal pathogens. Still, the biological basis for the pathophysiological distinction of the two disease categories has not been well documented yet. Type I NKT cells are a lymphocyte subset with important roles in regulating immune responses to either tolerance or immunity, including immune responses against bacterial pathogens. In this study, we delineate the mechanisms of NKT cell activation in periodontal infections. We show an infiltration of type I NKT cells in aggressive, but not chronic, periodontitis lesions in vivo. Murine dendritic cells infected with aggressive periodontitis-associated Aggregatibacter actinomycetemcomitans triggered a type I IFN response followed by type I NKT cell activation. In contrast, infection with Porphyromonas gingivalis, a principal pathogen in chronic periodontitis, did not induce NKT cell activation. This difference could be explained by the absence of a type I IFN response to P. gingivalis infection. We found these IFNs to be critical for NKT cell activation. Our study provides a conceivable biological distinction between the two periodontitis subforms and identifies factors required for the activation of the immune system in response to periodontal bacteria.
Department of Prostate Cancer Research, Institute of Pathology, University of Bonn, Bonn 53127, Germany. nowakm@uni-bonn.de
Michael
M
Nowak
Benjamin
B
Krämer
Manuela
M
Haupt
Panos N
PN
Papapanou
Justus
J
Kebschull
Per
P
Hoffmann
Ingo G
IG
Schmidt-Wolf
Søren
S
Jepsen
Peter
P
Brossart
Sven
S
Perner
Moritz
M
Kebschull
D000208:Acute Disease; D000328:Adult; D016976:Aggregatibacter actinomycetemcomitans / Q000276:immunology* / Q000472:pathogenicity; D000818:Animals; D001706:Biopsy; D002465:Cell Movement / Q000276:immunology; D002908:Chronic Disease; D003713:Dendritic Cells / Q000276:immunology / Q000382:microbiology / Q000473:pathology; D054884:Host-Pathogen Interactions; D006801:Humans; D007370:Interferon Type I / Q000096:biosynthesis / Q000276:immunology*; D008213:Lymphocyte Activation; D051379:Mice; D018345:Mice, Knockout; D055611:Natural Killer T-Cells / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D010518:Periodontitis / Q000276:immunology* / Q000382:microbiology* / Q000473:pathology; D016966:Porphyromonas gingivalis / Q000276:immunology*; D013045:Species Specificity
D007370:Interferon Type I