ADP‐heptose enables Helicobacter pylori to exploit macrophages as a survival niche by suppressing antigen‐presenting HLA‐II expression

Abstract excerpt

The persistence of Helicobacter pylori in the human gastric mucosa implies that the immune response fails to clear the infection. We found that H. pylori compromises the antigen presentation ability of macrophages, because of the decline of the presenting molecules HLA-II. Here, we reveal that the main bacterial factor responsible for this effect is ADP-heptose, an intermediate metabolite in the biosynthetic...

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