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However, the role of natural killer <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content> cells in the pathogenesis of periodontitis has not been clarified.<\/jats:p><\/jats:sec><jats:sec><jats:title>Materials and Methods<\/jats:title><jats:p>To examine the role of these cells, C57<jats:styled-content style=\"fixed-case\">BL<\/jats:styled-content>\/6J (wild\u2010type), <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>1d<jats:sup>\u2212\/\u2212<\/jats:sup> and \u03b1\u2010galactosylceramide (\u03b1<jats:styled-content style=\"fixed-case\">GC<\/jats:styled-content>)\u2010stimulated wild\u2010type mice were orally infected with <jats:italic><jats:styled-content style=\"fixed-case\">P<\/jats:styled-content>orphyromonas gingivalis<\/jats:italic> strain W83.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Apart from <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>1d<jats:sup>\u2212\/\u2212<\/jats:sup> mice, the level of alveolar bone resorption was elevated by the infection and was further accelerated in \u03b1<jats:styled-content style=\"fixed-case\">GC<\/jats:styled-content>\u2010stimulated mice. The infection induced elevated levels of serum amyloid <jats:styled-content style=\"fixed-case\">A<\/jats:styled-content> and <jats:italic><jats:styled-content style=\"fixed-case\">P<\/jats:styled-content>.\u00a0gingivalis<\/jats:italic>\u2010specific IgG in the sera, although the degree of elevation was much smaller in the <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>1d<jats:sup>\u2212\/\u2212<\/jats:sup> mice. Infection\u2010induced <jats:styled-content style=\"fixed-case\">RANKL<\/jats:styled-content> elevation was only observed in \u03b1<jats:styled-content style=\"fixed-case\">GC<\/jats:styled-content>\u2010stimulated mice. Although the cytokines produced by splenocytes were mainly <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>\u2010helper 1 type in wild\u2010type mice, those in \u03b1<jats:styled-content style=\"fixed-case\">GC<\/jats:styled-content>\u2010stimulated mice were predominantly <jats:styled-content style=\"fixed-case\">T\u2010<\/jats:styled-content>helper 2 type. In the liver, the infection demonstrated no effect on the gene expression for interferon\u2010\u03b3, interleukin\u20104 and <jats:styled-content style=\"fixed-case\">RANKL<\/jats:styled-content> except \u03b1<jats:styled-content style=\"fixed-case\">GC<\/jats:styled-content>\u2010stimulated mice in which the infection upregulated the gene expressions.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>This study is the first to show that natural killer <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content> cells upregulated systemic and local inflammatory responses induced by oral infection with <jats:italic><jats:styled-content style=\"fixed-case\">P<\/jats:styled-content>.\u00a0gingivalis<\/jats:italic>, thereby contributing to the progression of alveolar bone 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