Listeria Hijacks Host Enzyme to Bypass Immune Defenses
The pathogen uses the effector Internalin C to redirect the host enzyme CYLD, enabling its survival within epithelial cells.
Updated on Oct. 29, 2026 in Life Sciences
Researchers have identified a mechanism where the pathogen Listeria monocytogenes hijacks a host enzyme called CYLD to survive inside cells. This research-stage finding reveals how the bacterium uses its effector protein Internalin C to evade immune restriction.
Why it matters
Understanding how intracellular pathogens rewire host proteins to maintain infection is critical for developing new strategies against cell-to-cell spread. This study clarifies a specific molecular pathway that Listeria exploits to bypass the host immune system.
The effector Internalin C (InlC) redirects the host deubiquitinase CYLD to M1-linked linear ubiquitin chains located at the bacterial poles. This recruitment occurs during intracellular infection and is required to shield the pathogen from IFN-γ and RNF213-mediated restriction.
The players
Listeria monocytogenes
A foodborne bacterial pathogen that invades host cells and moves between them to avoid extracellular immune detection.
Internalin C
A secreted effector protein that the bacterium uses to manipulate host cell signaling pathways during infection.
CYLD
A host enzyme classified as a deubiquitinase that typically regulates cell survival and immune signaling.
RNF213
A host protein that acts as an intracellular sensor to detect and restrict the spread of bacterial pathogens.
The details
Listeria monocytogenes secretes the effector protein Internalin C (InlC) to physically capture the host enzyme CYLD, a deubiquitinase responsible for removing ubiquitin chains from proteins. By concentrating CYLD at the bacterial poles where M1-linked linear ubiquitin is present, the pathogen avoids the host's intracellular defense systems. This study used split-TurboID, a proximity-labeling tool that identifies interacting proteins, to map how CYLD is recruited to the pathogen's surface in epithelial cells.
Timeline
- 2026-10-29
The research findings were published.
The Tech Race
This research provides a new molecular explanation for how pathogens evade IFN-γ and RNF213-mediated host defenses. It shifts the current understanding of host-pathogen interactions from a simple recognition model to one involving active spatial reprogramming of host enzymes.
This is a basic science discovery at the cellular level and does not yet change clinical treatment for patients. Future research may utilize this pathway to develop targeted inhibitors that prevent pathogens from hijacking host immune machinery.
The takeaway
Pathogens like Listeria demonstrate the complexity of co-evolution by actively repurposing host enzymes to survive immune pressure. Watch for future studies investigating if small-molecule inhibitors can disrupt the InlC-CYLD interaction to sensitize bacteria to existing immune responses.
Further reading
Explore more breakthroughs in Life Sciences.
Source note: This article includes information reported by Nature.
