In tumors treated with type V adenovirus, thymosin alpha‑1 reprogrammed M2-like tumor-associated macrophages toward an antitumoral phenotype.
In plain wordsIn tumor models treated with a virus therapy, thymosin alpha‑1 shifted tumor immune cells from a tumor-helping state to an anti-tumor state.
- Peptide
- Thymosin alpha-1
- Outcome
- DecreaseM2-like tumor-associated macrophage phenotype
- Study
n: not reported in source
- Comparator
- Oncolytic adenovirus alone
- Outcome group
- Immune response · Cancer
- Studied dose
- Dose not stated
Source sentences
By selectively compensating for these deficiencies, thymosin alpha 1 (Tα1) reprograms "M2-like" TAMs toward an antitumoral phenotype, thereby reprogramming the TME into a state more beneficial for antitumor immunity.
1 context sentence(design, population, supporting numbers)
Here, we demonstrate that type V adenovirus (ADV) induces the polarization of tumor-associated macrophages (TAMs) to the M2 phenotype and increases the infiltration of regulatory T cells (Tregs) in the tumor microenvironment (TME).