Molecular signals in antigen presentation. I. Effects of interleukin 1 and 2 on radiation-treated antigen-presenting cells in vivo and in vitro.
In order to clarify the nature of the defect in the process of antigen presentation caused by uv radiation, low-density spleen cells were used as a potent APC source in a hapten-specific cytolytic T-cell (Tc) system. It was demonstrated that IA+ weakly adherent low-density spleen cells, when directly coupled with azobenzene arsonate (ABA), led to the activation ABA-specific Tc. When these APC were exposed to uv radiation (12 J/m2/sec) for 30 sec, their ability to lead to Tc activation was markedly inhibited. The defect imposed by uv radiation could be specifically bypassed by the addition of small amounts of homogeneous IL-1 or IL-2. This led to the specific activation of ABA-reactive H-2-restricted Tc. The purified IL-1 was also found to bypass the systemic defect imposed in vivo by external uv radiation of mice. This may indicate a potential therapeutic role for IL-1.
D000818:Animals; D000941:Antigens / Q000276:immunology*; D001152:Arsenicals / Q000494:pharmacology; D005260:Female; D007375:Interleukin-1 / Q000502:physiology*; D007376:Interleukin-2 / Q000502:physiology*; D051379:Mice; D008807:Mice, Inbred BALB C; D011946:Receptors, Antigen / Q000528:radiation effects*; D013601:T-Lymphocytes / Q000276:immunology; D013602:T-Lymphocytes, Cytotoxic / Q000187:drug effects; D014466:Ultraviolet Rays
D000941:Antigens; D001152:Arsenicals; D007375:Interleukin-1; D007376:Interleukin-2; D011946:Receptors, Antigen; C007492:dinitrophenyl-6-aminocaproyltyrosylazobenzene-4-arsonate