A stroma-sensing TGF-β blockade reprograms CAF-myeloid niches to induce durable tumor immunity.

In fibrotic, immune-excluded tumors, FN-EDB-targeted sTGF-βRII (FEBP-sTβRII) suppresses TGF-β/SMAD signaling and reprograms CAF–myeloid niches to enable durable, T cell–dependent tumor regression and long-term cross-protection.

• Why it matters: TGF-β accumulation in the tumor microenvironment blocks durable antitumor immunity, especially in fibrotic settings where immune cells are excluded.
• What they did: The study engineered a localized TGF-β inhibitor, FEBP-sTβRII, to bind FN-EDB-rich tumor matrix and tested its effects on TGF-β/SMAD signaling, T cell activation/IFN-γ production, and CAF–myeloid state.
• The result: FEBP-sTβRII relieves immune exclusion, sustains antigen-visible T cell infiltration and activation, expands effector-memory populations, and produces long-term, cross-protective immunity with fewer peripheral transcriptional disturbances than systemic sTβRII.

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