ORCID Profile
0000-0002-5184-6917
Current Organisation
Osaka University
Does something not look right? The information on this page has been harvested from data sources that may not be up to date. We continue to work with information providers to improve coverage and quality. To report an issue, use the Feedback Form.
Publisher: Royal Society of Chemistry (RSC)
Date: 2020
DOI: 10.1039/D0CC06263D
Abstract: Cholesteryl and ergosteryl 6- O -acyl-α- d -mannosides from Candida albicans signal through the innate immunity receptor Mincle.
Publisher: Rockefeller University Press
Date: 29-09-2020
DOI: 10.1084/JEM.20200815
Abstract: Helicobacter 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. Here, we report that H. pylori metabolites modified from host cholesterol exacerbate gastritis through the interaction with C-type lectin receptors. Cholesteryl acyl α-glucoside (αCAG) and cholesteryl phosphatidyl α-glucoside (αCPG) were identified as noncanonical ligands for Mincle (Clec4e) and DCAR (Clec4b1). During chronic infection, H. pylori–specific T cell responses and gastritis were ameliorated in Mincle-deficient mice, although bacterial burdens remained unchanged. Furthermore, a mutant H. pylori strain lacking αCAG and αCPG exhibited an impaired ability to cause gastritis. Thus H. pylori–specific modification of host cholesterol plays a pathophysiological role that exacerbates gastric inflammation by triggering C-type lectin receptors.
Publisher: Proceedings of the National Academy of Sciences
Date: 23-10-2018
Abstract: Group A Streptococcus (GAS) causes invasive streptococcal infections in humans, resulting in high mortality. Thus, GAS is also known as “killer bacteria” or “flesh-eating bacteria.” The mechanism by which the immune system recognizes this potent pathogen remains elusive. In this study, we showed that the innate immune receptor Mincle (macrophage inducible C-type lectin) plays pivotal roles against invasive GAS infection through the recognition of monoglucosyldiacylglycerol (MGDG), a component of the lipoteichoic acid anchor. MGDG induced proinflammatory cytokines, ROS, and NO production in a Mincle-dependent manner. In an invasive GAS infection model, Mincle-deficient mice exhibited severe bacteremia and rapid lethality. These results indicate that Mincle plays a central role in protective immunity against acute GAS infection.
Location: Japan
No related grants have been discovered for Sho Yamasaki.