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ATP and control of intracellular growth of mycobacteria by T cells
David H Canaday1, Reza Beigi, Richard F Silver
1Department of Medicine, University Hospitals of Cleveland and Case Western Reserve University, Cleveland, Ohio 44109, USA. dxc44@cwru.edu
Abstract:
Extracellular ATP at millimolar concentrations inhibits growth of mycobacteria in human macrophages. Whether T cells can produce sufficient ATP is unknown. CD4(+) and CD8(+) T cells did not release sufficient ATP through either degranulation or lysis of bystander cells to restrict growth of Mycobacterium bovis BCG in monocytes.
Insights
Extracellular adenosine triphosphate (ATP) can inhibit mycobacteria growth in macrophages. However, T cells do not release enough ATP to restrict Mycobacterium bovis BCG growth in monocytes.
Area of Science:
- Immunology
- Cellular Biology
- Microbiology
Background:
- Extracellular adenosine triphosphate (ATP) at millimolar concentrations has been shown to inhibit the growth of mycobacteria within human macrophages.
- The capacity of T cells to produce and release sufficient ATP to influence mycobacterial growth remains largely unknown.
Purpose of the Study:
- To investigate whether T cells can produce and release adequate levels of extracellular ATP to inhibit the growth of Mycobacterium bovis Bacillus Calmette-Guérin (BCG) in human monocytes.
Main Methods:
- Analysis of ATP release from CD4(+) and CD8(+) T cells.
- Assessment of the impact of T cell-derived ATP on Mycobacterium bovis BCG growth in co-cultured human monocytes.
Main Results:
- CD4(+) and CD8(+) T cells were found to release insufficient amounts of extracellular ATP.
- The ATP released by T cells, whether through degranulation or lysis of bystander cells, did not significantly restrict the growth of Mycobacterium bovis BCG in monocytes.
Conclusions:
- T cells do not appear to be a significant source of extracellular ATP capable of inhibiting mycobacterial growth in monocytes.
- The findings suggest that mechanisms other than T cell-mediated ATP release are primarily responsible for controlling mycobacterial infections in macrophages.