The Helicobacter pylori HopQ outermembrane protein inhibits immune cell activities

Chamutal Gur*, Naseem Maalouf, Markus Gerhard, Bernhard B. Singer, Johanna Emgård, Violeta Temper, Tzahi Neuman, Ofer Mandelboim, Gilad Bachrach

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

35 Scopus citations


We previously showed that the colorectal cancer colonizing bacterium Fusobacterium nucleatum protects tumors from immune cell attack via binding of the fusbacterial Fap2 outer-membrane protein to TIGIT, a checkpoint inhibitory receptor expressed on T cells and NK cells. Helicobacter pylori, the causative agent for peptic ulcer disease, is associated with the development of gastric adenocarcinoma and MALT lymphoma. The HopQ outer-membrane adhesin of H. pylori was recently shown to bind carcinoembryonic antigen-related cell adhesion molecules (CEACAMs) including CEACAM1, an inhibitory receptor expressed mainly by activated T and NK cells. Here we investigated the possibility that similar to Fap2, HopQ can also inhibit immune cell activities by interacting with CEACAM1. We used several approaches to confirm that HopQ indeed interacts with CEACAM1, and show that CEACAM1-mediated activation by HopQ, may inhibit NK and T cell functions.

Original languageAmerican English
Article numbere1553487
Issue number4
StatePublished - 3 Apr 2019

Bibliographical note

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© 2019, © 2019 Taylor & Francis Group, LLC.


  • Helicobacter pylori
  • immune cells


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