University at Buffalo - The State University of New York
Skip to Content
A bacterial glycan core linked to surface (S)-layer proteins modulates host immunity through Th17 suppression. - PubMed - NCBI

Send to

Choose Destination
See comment in PubMed Commons below
Mucosal Immunol. 2013 Mar;6(2):415-26. doi: 10.1038/mi.2012.85. Epub 2012 Sep 12.

A bacterial glycan core linked to surface (S)-layer proteins modulates host immunity through Th17 suppression.

Author information

Department of Oral Biology, School of Dental Medicine, University at Buffalo, State University of New York, Buffalo, New York, USA.


Tannerella forsythia is a pathogen implicated in periodontitis, an inflammatory disease of the tooth-supporting tissues often leading to tooth loss. This key periodontal pathogen is decorated with a unique glycan core O-glycosidically linked to the bacterium's proteinaceous surface (S)-layer lattice and other glycoproteins. Herein, we show that the terminal motif of this glycan core acts to modulate dendritic cell effector functions to suppress T-helper (Th)17 responses. In contrast to the wild-type bacterial strain, infection with a mutant strain lacking the complete S-layer glycan core induced robust Th17 and reduced periodontal bone loss in mice. Our findings demonstrate that surface glycosylation of this pathogen may act to ensure its persistence in the host likely through suppression of Th17 responses. In addition, our data suggest that the bacterium then induces the Toll-like receptor 2-Th2 inflammatory axis that has previously been shown to cause bone destruction. Our study provides a biological basis for pathogenesis and opens opportunities in exploiting bacterial glycans as therapeutic targets against periodontitis and a range of other infectious diseases.

[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Nature Publishing Group Icon for PubMed Central
    Loading ...
    Support Center