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Updated: Jun 25, 2026
08:32
Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
Published on: March 2, 2014
Viral subversion of immunogenic cell death.
Oliver Kepp1, Laura Senovilla, Lorenzo Galluzzi
1INSERM, U848, Villejuif, France.
Cell Cycle (Georgetown, Tex.)
|February 18, 2009
Summary
Pathogen-induced cell death can trigger immune responses by exposing calreticulin (CRT) on cell surfaces. Viruses may prevent this "eat-me" signal, thus evading immune detection and promoting infection.
Area of Science:
- Immunology
- Cell Biology
- Virology
Background:
- Physiological cell death is typically non-immunogenic.
- Pathogen-induced cell death can elicit immune responses against cellular antigens.
- Immunogenic cell death exposes calreticulin (CRT) as an "eat-me" signal for dendritic cells (DCs).
Purpose of the Study:
- To investigate the mechanisms of calreticulin (CRT) exposure during immunogenic cell death.
- To explore how viruses may subvert CRT exposure to evade immune detection.
Main Methods:
- Analysis of the CRT translocation pathway involving ER stress response, apoptosis machinery, and exocytosis.
- Investigation of viral proteins that interfere with CRT exposure pathways.
Main Results:
- CRT exposure is a hallmark of immunogenic apoptosis, facilitating DC engulfment.
- CRT translocation involves ER stress (PERK), apoptosis (caspase-8, BAP31, Bax, Bak), and vesicular transport.
- Viruses possess proteins that inhibit key components of the CRT exposure pathway.
Conclusions:
- Obligate intracellular pathogens likely employ strategies to inhibit CRT exposure.
- Subversion of CRT exposure allows pathogens to avoid immunogenic cell death and subsequent immune responses.
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