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The Helicobacter pylori HopQ outermembrane protein inhibits immune cell activities

Chamutal Gur1, Naseem Maalouf2, Markus Gerhard3

  • 1The Lautenberg center for immunology and cancer research, The Hebrew University Hadassah Medical School, Institute for Medical Research Israel-Canada (IMRIC), Jerusalem, Israel.

Oncoimmunology
|March 26, 2019
PubMed

Insights

The bacterium Helicobacter pylori uses its HopQ protein to interact with CEACAM1 on immune cells. This interaction may suppress T and NK cell functions, similar to how Fusobacterium nucleatum affects tumors.

Area of Science:

  • Microbiology
  • Immunology
  • Cancer Research

Background:

  • Fusobacterium nucleatum's Fap2 protein inhibits TIGIT on immune cells, protecting colorectal tumors.
  • Helicobacter pylori is linked to gastric cancer and uses HopQ to bind CEACAMs.

Purpose of the Study:

  • To investigate if Helicobacter pylori's HopQ protein inhibits immune cell activity by binding CEACAM1.
  • To explore the potential immune-suppressive role of the HopQ-CEACAM1 interaction.

Main Methods:

  • Biochemical assays to confirm HopQ-CEACAM1 interaction.
  • Functional assays to assess NK and T cell responses upon HopQ engagement with CEACAM1.

Main Results:

  • Confirmed that the HopQ adhesin of H. pylori directly interacts with CEACAM1.
  • Demonstrated that CEACAM1 engagement by HopQ can inhibit NK and T cell functions.

Conclusions:

  • HopQ-mediated CEACAM1 binding by H. pylori may contribute to immune evasion in gastric cancer.
  • This mechanism is analogous to Fap2-TIGIT interaction by F. nucleatum, highlighting convergent bacterial immune evasion strategies.
Keywords:
CEACAM1Helicobacter pyloriimmune cells

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