1932

Abstract

▪ Abstract 

Immune cell–mediated destruction of pathogens may result in excessive collateral damage to normal tissues, and the failure to control activated immune cells may cause immunopathologies. The search for physiological mechanisms that downregulate activated immune cells has revealed a critical role for extracellular adenosine and for immunosuppressive A adenosine receptors in protecting tissue from inflammatory damage. Tissue damage–associated deep hypoxia, hypoxia-inducible factors, and hypoxia-induced accumulation of adenosine may represent one of the most fundamental and immediate tissue-protecting mechanisms, with adenosine A receptors triggering “OFF” signals in activated immune cells. In these regulatory mechanisms, oxygen deprivation and extracellular adenosine accumulation serve as “reporters,” while A adenosine receptors serve as “sensors” of excessive tissue damage. The A receptor–triggered generation of intracellular cAMP then inhibits activated immune cells in a delayed negative feedback manner to prevent additional tissue damage. Targeting A adenosine receptors may have important clinical applications.

Loading

Article metrics loading...

/content/journals/10.1146/annurev.immunol.22.012703.104731
2004-04-23
2024-03-29
Loading full text...

Full text loading...

/content/journals/10.1146/annurev.immunol.22.012703.104731
Loading
/content/journals/10.1146/annurev.immunol.22.012703.104731
Loading

Data & Media loading...

  • Article Type: Review Article
This is a required field
Please enter a valid email address
Approval was a Success
Invalid data
An Error Occurred
Approval was partially successful, following selected items could not be processed due to error