In mice with weak immune systems, giving thymosin‑alpha‑1 a couple of times a week raised the amount of a signaling protein called IL‑3, which helps blood‑forming cells grow, but it didn’t raise IL‑2, another key immune signal. The effect was seen only in the sick mice, not in normal healthy ones, suggesting the peptide works early in T‑cell development and may aid immune recovery rather than boost a healthy immune system.

Thymosin-alpha 1 increased the capability of nu/nu mice to produce interleukin (IL)-3 but not IL-2 when administered intraperitoneally at doses of 0.5 and 5.0 micrograms/kg twice a week for 3-6 weeks. Thy-1-positive cells were responsible for the production of IL-3, which was determined by proliferation of the IL-3-dependent cell line (FDC-P2) as well as by augmentation of the in vitro growth of hematopoietic stem cells (colony-forming unit S [CFU-S]). The IL-3 activity released by nu/nu splenocytes emerged in fractions coincidentally with IL-3 released by WEHI-3 cells on Mono Q anion-exchange chromatography. However, IL-2 activity determined by proliferation of the IL-2-dependent cell line was not detected in any fractions of the same chromatography. These findings indicate that IL-2 is not always coproduced with IL-3 by Thy-1-positive cells. This suggests, taken together with results from previous studies about the cells producing IL-2 and IL-3 by other investigators, that thymosin-alpha 1 exerts its effect at an early stage of T cell differentiation to induce a T cell subpopulation capable of producing IL-3 (but not yet IL-2). Based on the present findings, we discuss the mechanism of action by which thymosin-alpha 1 exerts its diverse effects in immunosuppressed hosts but not a potentiating effect in healthy normal animals or in in vitro assays of T cell function.