TY - JOUR
T1 - Activation of invariant NK T cells in periodontitis lesions
AU - Nowak, Michael
AU - Krämer, Benjamin
AU - Haupt, Manuela
AU - Papapanou, Panos N.
AU - Kebschull, Justus
AU - Hoffmann, Per
AU - Schmidt-Wolf, Ingo G.
AU - Jepsen, Søeren
AU - Brossart, Peter
AU - Perner, Sven
AU - Kebschull, Moritz
N1 - Copyright:
Copyright 2013 Elsevier B.V., All rights reserved.
PY - 2013/3/1
Y1 - 2013/3/1
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=84874228511&partnerID=8YFLogxK
U2 - 10.4049/jimmunol.1201215
DO - 10.4049/jimmunol.1201215
M3 - Journal articles
C2 - 23365081
AN - SCOPUS:84874228511
SN - 0022-1767
VL - 190
SP - 2282
EP - 2291
JO - Journal of Immunology
JF - Journal of Immunology
IS - 5
ER -