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Altered cell signaling and mononuclear phagocyte deactivation during intracellular infection
1Dept of Medicine, University of British Columbia Faculties of Medicine, Vancouver, Canada.
Abstract:
Given the critical antimicrobial properties of mononuclear phagocytes, an important concern in cell biology and immunology has been to understand how intracellular microbes are able to establish states of chronic infection within these cells. Recent studies indicate that mononuclear phagocytes become functionally deactivated during intracellular infection. Here, Neil Reiner considers the experimental evidence to indicate that this is a frequent event that may be accounted for by induced defects in the signaling pathways required to bring cells to an activated state.
Insights
Intracellular microbes can cause chronic infections by deactivating mononuclear phagocytes. This study reviews evidence suggesting that infection-induced signaling defects lead to this functional deactivation, hindering the immune response.
Area of Science:
- Cell biology
- Immunology
- Microbiology
Background:
- Mononuclear phagocytes possess crucial antimicrobial functions.
- Understanding how intracellular microbes establish chronic infections within these cells is a key research area.
Purpose of the Study:
- To review experimental evidence on the functional deactivation of mononuclear phagocytes during intracellular infection.
- To explore the mechanisms underlying this deactivation, focusing on signaling pathways.
Main Methods:
- Review of existing experimental studies on mononuclear phagocyte function and intracellular infections.
- Analysis of signaling pathways implicated in cellular activation and immune response.
Main Results:
- Evidence suggests that functional deactivation of mononuclear phagocytes is a frequent event during chronic intracellular infections.
- This deactivation appears to be caused by induced defects in signaling pathways essential for cell activation.
Conclusions:
- Intracellular microbial infections can impair the host's immune cells.
- Targeting these induced signaling defects may offer strategies to restore mononuclear phagocyte function and combat chronic infections.