The effects of corticosteroid hormones and thyroid hormones on lymphocyte viability and proliferation during development and metamorphosis of Xenopus laevis.
Metamorphosis in the South African clawed frog, Xenopus laevis, is characterized by a striking loss of lymphocytes in the thymus, liver, and spleen. Changes in the proliferative responses of splenocytes and thymocytes to T cell mitogens and semi-allogeneic cells are also observed at metamorphosis. Because the levels of circulating thyroid hormones (TH) and corticosteroid hormones (CH) increase dramatically during the climax of metamorphosis, we have investigated the possible role of TH and CH as mediators of the changes in lymphocyte numbers or lymphocyte function. Here we report on the in vitro effects of CH and TH on lymphocyte viability and on phytohemagglutinin-P (PHA)-stimulated lymphocyte proliferation at prometamorphosis and climax of metamorphosis. We have observed consistently significant inhibition of proliferation by corticosterone. In contrast, we have observed inconsistent inhibition of proliferation by both thyroxine (T4) and triiodothyronine (T3). In short-term studies, the viability of thymocytes and splenocytes was reduced in the presence of CH but not TH. These observations are consistent with a hypothesis that loss of larval lymphocytes and changes of lymphocyte function at metamorphosis may be due to elevated concentrations of CH rather than TH. Because CH have been shown to enhance TH-induced effects during metamorphosis, we looked at the combined effects of these agents on PHA-stimulated lymphocyte proliferation. While each agent was inhibitory in several experiments, there was no significantly greater inhibition when splenic lymphocytes were cultured with both.
Rollins-Smith
L A
LA
Department of Microbiology & Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232.
Blair
P J
PJ
D000305:Adrenal Cortex Hormones / Q000494:pharmacology*; D000818:Animals; D002455:Cell Division / Q000187:drug effects / Q000502:physiology; D002470:Cell Survival / Q000187:drug effects / Q000502:physiology; D002478:Cells, Cultured; D003345:Corticosterone / Q000494:pharmacology; D007814:Larva / Q000166:cytology / Q000502:physiology; D008214:Lymphocytes / Q000166:cytology* / Q000187:drug effects / Q000502:physiology; D008675:Metamorphosis, Biological / Q000187:drug effects / Q000502:physiology*; D010472:Perchlorates / Q000494:pharmacology; D010835:Phytohemagglutinins / Q000494:pharmacology; D017670:Sodium Compounds / Q000494:pharmacology; D013154:Spleen / Q000166:cytology / Q000502:physiology; D013961:Thyroid Gland / Q000166:cytology / Q000502:physiology; D013963:Thyroid Hormones / Q000494:pharmacology*; D013974:Thyroxine / Q000494:pharmacology; D014284:Triiodothyronine / Q000494:pharmacology; D014982:Xenopus laevis / Q000502:physiology*
D000305:Adrenal Cortex Hormones; D010472:Perchlorates; D010835:Phytohemagglutinins; D017670:Sodium Compounds; D013963:Thyroid Hormones; D014284:Triiodothyronine; C031068:sodium perchlorate; D013974:Thyroxine; D003345:Corticosterone