2010 Fiscal Year Final Research Report
P.gingivalis target DC-SIGN to escape Th1-type immune response.
Project/Area Number |
21792108
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Single-year Grants |
Research Field |
Periodontal dentistry
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Research Institution | Tohoku University |
Principal Investigator |
TADA Hiroyuki Tohoku University, 病院, 医員 (70431632)
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Project Period (FY) |
2009 – 2010
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Keywords | 免疫学 / 樹状細胞 / 細胞・組織 / サイトカイン / DC-SIGN |
Research Abstract |
Dendritic cells (DCs) express C-type lectin receptors (CLRs). Pathogenic bacteria subvert DC functions to escape immune surveillance by targeting the CLRs including DC-SIGN. In this study, we investigated the role played by Nod proteins in inducing the cross-priming of CD8^+T cells, and we demonstrate that Nod ligands significantly enhance the induction of DC-mediated cross-priming.
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