Thymosin alpha 1 restores NK-cell activity and prevents tumor progression in mice immunosuppressed by cytostatics or X-rays.
Umeda. Y Y; Sakamoto. A A; Nakamura. J J; Ishitsuka. H H; Yagi. Y Y
Key Findings
- Thymosin‑alpha‑1 given with or after chemo/radiation kept NK‑cell activity from dropping in mice
- Mice that got thymosin‑alpha‑1 survived longer than those that didn’t, though they eventually died from leukemia
- The protective effect depended on NK cells, as removing NK cells blocked the benefit
Practical Outcomes
- Thymosin‑alpha‑1 might be useful as an immune‑support supplement during periods of chemotherapy or radiation, but the data are only from mice and no human dosing or safety info is available. For biohackers, it suggests a potential way to protect NK cells, but any use should be experimental, under medical supervision, and not expected to cure cancer.
Summary
In mouse experiments, giving the peptide thymosin‑alpha‑1 helped keep natural killer (NK) immune cells working after the animals were weakened by chemotherapy drugs or X‑ray radiation, which let them survive longer before their leukemia took over. The benefit seemed to come from NK cells, not other immune cells.
Abstract
The effect of thymosin against tumor progression was examined in mice immunosuppressed by cytostatics or X-ray irradiation. When pretreated with cytostatic agents, such as 5-fluorouracil (5-FU) or BCNU, or by X-ray, and then inoculated with P388 or L1210 leukemias, mice died rapidly within a few days. In these systems, thymosin alpha 1 given concomitantly with the cytostatic agents or after X-irradiation prevented rapid death and extended survival, although the mice eventually died with leukemia like normal mice inoculated with cells of the same tumor. Rapid death in the 5-FU-treated mice was also prevented by adoptive transfer of spleen cells from the donor mice if these had been treated with 5-FU plus thymosin alpha 1, but not if they had received 5-FU alone. However, the restorative activity of the donor spleen cells was abrogated by treatment with anti-asialo GM1, but not by treatment with anti-Thy 1 or anti-mouse Ig serum, suggesting that the effector cells in the spleen are NK cells. In fact, thymosin alpha 1, when given concomitantly with 5-FU or after X-irradiation, maintained the NK activity of spleen, which was damaged by treatment with 5-FU or X-irradiation alone. The present study indicates that thymosin alpha 1 exerts a preventive activity against progression of leukemias at least in part through an effect on NK cells or their progenitor cells.
Study Information
pubmed
1983
10.1007/bf00199694