Related Experiment Videos
Taking the Myc is bad for Theileria
Frédéric Dessauge1, Regina Lizundia, Martin Baumgartner
1Laboratoire de Biologie Cellulaire Comparative des Apicomplexes, UMR 8104 CNRS/U567 INSERM, Département Maladies Infectieuses, Hôpital Cochin-Batiment Gustave Roussy, 75014 Paris, France.
Trends in Parasitology
|June 28, 2005
Summary
Intracellular parasites like Theileria hijack host cell survival. Theileria parva infection of bovine B cells induces c-Myc, activating Mcl-1 to prevent programmed cell death and ensure parasite survival.
Area of Science:
- Parasitology
- Cell Biology
- Immunology
Background:
- Intracellular parasites manipulate host cell survival pathways.
- Theileria parasites invade bovine leukocytes, immortalizing them.
- Host cell survival is essential for parasite viability; parasite death triggers host cell apoptosis.
Purpose of the Study:
- To investigate the mechanisms by which Theileria parasites ensure host cell survival.
- To identify specific host cell pathways manipulated by Theileria parva in B cells.
Main Methods:
- Analysis of host cell gene expression and protein activation in infected leukocytes.
- Focus on the role of c-Myc and Mcl-1 in parasite-mediated cell survival.
Main Results:
- Theileria parva infection induces c-Myc expression in bovine B cells.
- Induced c-Myc leads to the activation of the anti-apoptotic protein Mcl-1.
- This pathway promotes host cell survival, essential for the parasite.
Conclusions:
- Theileria parasites utilize host cell machinery, specifically the c-Myc/Mcl-1 axis, to prevent apoptosis.
- This mechanism ensures parasite survival by maintaining a viable host cell.
- Similar parasitic manipulation strategies may exist in other leukocyte types and host-parasite systems.