AI Article Synopsis
- Autophagy is a key process that helps cells degrade damaged components and keep themselves healthy by breaking down long-lived proteins and organelles.
- The Th1 cytokine IFN-gamma boosts autophagy in macrophages, helping them fight off infections by Mycobacterium tuberculosis, which tries to survive by preventing the fusion of phagosomes and lysosomes.
- In contrast, Th2 cytokines like IL-4 and IL-13 can suppress autophagy in macrophages, influencing how the immune system responds to mycobacterial infections.
Article Abstract
Autophagy is a major intracellular pathway for the lysosomal degradation of long-lived cytoplasmic macromolecules and damaged or surplus organelles. More recently, autophagy has also been linked with innate and adaptive immune responses against intracellular pathogens, including Mycobacterium tuberculosis, which can survive within macrophages by blocking fusion of the phagosome with lysosomes. Induction of autophagy by the Th1 cytokine IFN-gamma enables infected macrophages to overcome this phagosome maturation block and inhibit the intracellular survival of mycobacteria. Conversely, the Th2 cytokines IL-4 and IL-13 inhibit autophagy in murine and human macrophages. We discuss how differential modulation of autophagy by Th1 and Th2 cytokines may represent an important feature of the host response to mycobacteria.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2789833 | PMC |
| http://dx.doi.org/10.1016/j.vetimm.2008.10.293 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!