What question did this study set out to answer?

To investigate the role of the Fgl2-FcγRIIB signaling pathway in activating myeloid-derived suppressor cells within the tumor microenvironment.

March 26, 2026Advanced ScienceOpen Access

Tumor‐Derived Exosomes Deliver Membrane‐Bound Fgl2 to Activate FcγRIIB‐Mediated Immunosuppression in Myeloid‐Derived Suppressor Cells

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Demonstrates how tumor-derived exosomes activate myeloid-derived suppressor cells, suggesting a new target for cancer treatment.

To investigate the role of the Fgl2-FcγRIIB signaling pathway in activating myeloid-derived suppressor cells within the tumor microenvironment.
Analyzed clinical specimens for Fgl2 expression and CD8+ T cell infiltration.
Assessed the internalization of tumor-derived exosomes by MDSCs.
Evaluated the effects of FcγRIIB genetic ablation and Fgl2 neutralization.
Tested a therapeutic strategy combining exosome secretion inhibitors with PD-L1 blockade.
Fgl2 expression is elevated in tumor tissues and inversely correlates with CD8+ T cell presence.
Tumor-derived exosomes were shown to deliver membrane-bound Fgl2 to MDSCs, enhancing their immunosuppressive function.
Genetic removal of FcγRIIB or Fgl2 neutralization restored T cell activity and reduced tumor growth.
Combined therapeutic strategies demonstrated significant antitumor effects.

Lin et al. (2026) studied this question.

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