A T cell model for age-related loss of homeostasis: identification of the cell type responsible for age-related delay in recovery of the PHA-induced mitogenic response from radiation injury.
Immunologic recovery from radiation injury was used to assess age-related loss of immunologic homeostasis. Mice were exposed to 500 rad to determine whether macrophages, T helper cells and/or T responder cells were responsible for the age-related delay in recovery of PHA-induced mitogenesis. Recovery of macrophages was determined by facilitation of macrophage-deficient cultures, recovery of T helper cells by interleukin 2 production, and recovery of T responder cells by incorporation of tritiated thymidine. The results showed that in old mice macrophages are resistant to radiation and aging, T helper cells recover completely from radiation, and recovery is incomplete for T responder cells.
D000375:Aging / Q000097:blood*; D000818:Animals; D002450:Cell Communication / Q000187:drug effects; D006706:Homeostasis / Q000528:radiation effects*; D007376:Interleukin-2 / Q000494:pharmacology; D008213:Lymphocyte Activation / Q000187:drug effects / Q000528:radiation effects*; D008264:Macrophages / Q000502:physiology / Q000528:radiation effects; D051379:Mice; D008815:Mice, Inbred Strains; D010835:Phytohemagglutinins / Q000494:pharmacology*; D011833:Radiation Injuries, Experimental / Q000097:blood*; D013154:Spleen / Q000166:cytology / Q000528:radiation effects; D013601:T-Lymphocytes / Q000145:classification / Q000276:immunology* / Q000528:radiation effects; D006377:T-Lymphocytes, Helper-Inducer / Q000528:radiation effects
D007376:Interleukin-2; D010835:Phytohemagglutinins