Thyroid status modulates the in vivo antitumor response to T lymphoma cells (P2079)

Abstract We have previously observed the regulation of immunity by thyroid status but little is known on how the levels of thyroid hormones (THs) influence antitumor responses. Our aim was to evaluate the antitumor immune response in hyper- and hypothyroid C57BL/6 mice (Hyper and Hypo respectively) which develop solid tumors and metastases in response to inoculation with EL-4 T lymphoma. Hyper showed increased rate of tumor growth compared to Hypo and control mice (C), while Hypo showed more metastases than other groups. Hyper Solid tumors had increased expression of cyclin D1, D3, E1, while Hypo had higher levels of cell cycle inhibitors p27, p16 and p53. At day 10th after EL-4 cell inoculation, when differences in tumor growth were significant, Hyper displayed higher number of cells in lymph nodes and spleens, a lower percentage (%) of myeloid-derived suppressor cells and an increased % of NK cells in the spleen accompanied by an augmented NK cell cytotoxic activity. On the other hand, Hypo displayed a reduction of CD8+ T cells and a decrease in tumor-specific cytotoxic activity. However, there were no differences among the groups in the % of T, B or Treg cells in secondary lymphoid organs. Our results suggest that THs modulate tumor growth through mechanisms involving regulation of proteins related to the progression and/or arrest of the cell cycle, and through the control of the anti-tumor immune response that could limit tumor dissemination.