S100A4 Is a Targetable Regulator of Immune Suppression in Glioblastoma

In mouse models of glioblastoma, inhibiting S100A4 reprograms the tumor microenvironment into an immunotherapy-responsive state, improving CD8 T cell activity and survival.

• Why it matters: GBM resists immunotherapy because its tumor microenvironment is profoundly immunosuppressive, limiting effective T cell infiltration and antigen presentation.
• What they did: The study used genetic knockdown of S100a4 in glioma cells and tested a novel S100A4/Transferrin Receptor bispecific antibody, including combinations with PD-1 blockade.
• The result: S100a4 inhibition increased CD8 T cell infiltration and effector function, promoted antigen-presenting cell maturation, and delivered significant survival benefits across GBM molecular subtypes, with BsA+anti-PD1 inducing tertiary lymphoid-like structures.

AI summary of the abstract · may contain errors · not medical advice · read the paper.