Meeting Abstract
Metamorphosis in anurans is accompanied by a dramatic loss of larval thymocytes as a new adult antibody repertoire is formed. Rising levels of glucocorticoids during metamorphosis have been shown to inhibit lymphocyte proliferation and induce thymus lymphocyte cell death. We have previously shown that treatment of tadpoles with exogenous thyroid hormone (T3, 5 nM) and the cortisol analog, dexamethasone (DEX, 2 uM), each separately induce thymus involution and apoptosis, and together exhibit a synergistic effect that accelerates these processes. To determine if each hormone affects the thymus directly, we cultured Nieuwkoop-Faber (NF) stage 54 thymus gland explants in the presence of either hormone. After 3 days of culture with DEX or T3, thymus gland surface areas decreased by 22% and 12% respectively (compared with no change in controls), indicating that each hormone affects the thymus directly. Using antibodies against epithelial-cadherin, active caspase-3 and phosphohistone-H3, we mapped thymus epithelial tissue, cell death, and proliferation (respectively) in thymus gland sections from NF54 tadpoles treated with either T3 or DEX. Proliferating cells were still present following T3 treatment, but completely absent following DEX treatment. Cell death and proliferation (when present) appeared to be confined to non-epithelial tissue (most likely T-cells). Our findings suggest that thymocyte cell death is induced directly by both T3 and DEX. In contrast, thymocyte proliferation is completely inhibited by DEX, but not by T3. We hypothesize that during natural metamorphosis thyroid hormones (TH) and glucocorticoids work synergistically to induce larval thymocyte apoptosis, and that TH simultaneously induces adult thymocyte proliferation.
