T cell potentiation by low dose ionizing radiation: possible mechanisms.
The phenomenon of a stimulatory response induced by an exposure to a low dose of an otherwise toxic agent has been observed in a wide variety of organisms, ranging from the simplest prokaryotes to higher eukaryotes and with a spectrum of stimuli. This would suggest that the phenomenon is evolutionarily conserved and biologically important. However, we do not understand the mechanism responsible for the phenomenon, although it has been known for over 100 y. A reasonable assumption would be that adequate models and challenging paradigms are lacking to resolve this fundamental problem. Evidence is presented to show that the potentiation of T cell response by exposing them to single or multiple low doses of ionizing radiation is a feasible cellular model to understand the phenomenon. In addition, several possible mechanisms are discussed, including the participation of stress proteins and prostaglandins in stabilizing the signal transducing, transcriptional and translational machineries, and the possible role of a more efficient mechanism of DNA repair.
Makinodan
T
T
Geriatric Research, Education and Clinical Center, VA Medical Center, West Los Angeles, CA 90073.
James
S J
SJ
D000818:Animals; D002470:Cell Survival / Q000528:radiation effects; D004249:DNA Damage; D004260:DNA Repair; D004307:Dose-Response Relationship, Radiation; D006360:Heat-Shock Proteins / Q000378:metabolism; D008213:Lymphocyte Activation / Q000528:radiation effects; D051379:Mice; D008810:Mice, Inbred C57BL; D011453:Prostaglandins / Q000502:physiology; D011829:Radiation Dosage; D013601:T-Lymphocytes / Q000276:immunology / Q000502:physiology / Q000528:radiation effects*; D013937:Thymidine Kinase / Q000378:metabolism / Q000528:radiation effects
D006360:Heat-Shock Proteins; D011453:Prostaglandins; D013937:Thymidine Kinase