The study shows that thymosin‑alpha‑1 can change mouse immune cells called dendritic cells, making them show more activation signals and less of an inflammatory molecule (IL‑12) when an inflammation signal (TNF‑alpha) is present, while still keeping their ability to activate T‑cells. However, this was done in a dish with mouse cells at high drug levels, so it doesn’t give clear guidance for human use yet.

Thymosin alpha 1 (Talpha1) has immunomodulatory effects on T-cells, NK-cells and macrophages, but its action on dendritic cells (DCs), which are recognized as the sole professional antigen presenting cells (APCs) capable of priming naïve T-cells, is poorly understood. In this study, the effect of Talpha1 in vitro on murine bone marrow-derived DCs (BMDCs) maturation, differentiation, and function with or without tumor necrosis factor-alpha (TNF-alpha), which is one of the important inflammatory parameters, has been investigated. We have shown, through flow cytometry, ELISA and mixed leukocyte reaction (MLR), that Talpha1 promoted CD4-expressed DC differentiation and the expression of activation markers, but did not influence IL-12 production and T cell-stimulatory capacity of DCs in the absence of TNFalpha during BMDCs maturation. Furthermore, in the presence of TNF-alpha, Talpha1 has been shown not only to promote the expression of CD4 on MHC class II+ DCs and enhance the up-regulated levels of mature markers induced by TNF-alpha, but also to suppress the up-regulated IL-12 production. Particularly, thus effects seen were obvious at pharmacological Talpha1 concentrations. However, Talpha1 did not inhibit TNF-alpha-induced T-cell stimulating function of DCs. This is the first reported example of a direct Talpha1-DC interaction and suggests a mechanism by which Talpha1 may in part affect T-cell responses by acting at the DC level and it may play an important role in the modulation of the local inflammatory responses in vivo.