Alberto Mantovani

Alberto Mantovani characterized the bidirectional crosstalk between tumor-associated macrophages and CAFs, demonstrating that inflammatory CAFs recruit and polarize macrophages toward immunosuppressive M2 phenotypes through CCL2, CXCL12, and IL-6, while M2 macrophages reciprocally activate fibroblasts into tumor-promoting CAFs through TGF-beta and PDGF, creating a self-reinforcing immunosuppressive circuit. His work on the complement system in the tumor stroma revealed that CAF-derived complement components activate both innate immune cells and cancer cells through C3a and C5a receptor signaling. He targets the myeloid-CAF immunosuppressive axis as a strategy to unlock anti-tumor immunity in stroma-rich cancers.