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Helicobacter pylori metabolites exacerbate gastritis through C-type lectin receptors (Yamasaki G, in JEM)

Helicobacter pylori (H. pylori) causes gastritis, which has been attributed to the development of H. pylori-specific T cells during infection. However, the mechanism underlying innate immune detection leading to the priming of T cells is not fully understood, as H. pylori evades TLR detection.

The research group of Sho Yamasaki (Molecular Immunology, IFReC/RIMD, Osaka University) revealed H. pylori metabolites modified from host cholesterol exacerbate gastritis through the interaction with C-type lectin receptors.


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Article (External Link)


Contact:
Molecular Immunology Sho Yamasaki

Sho Yamasaki(Molecular Immunology)


Tel+81-6-6879-8306
Mailyamasakibiken.osaka-u.ac.jp

Immunology Frontier Research Center, Osaka University (WPI-IFReC)

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