Tissue-resident FOLR2+ macrophages associate with tumor-infiltrating CD8+ T cells and with increased survival of breast cancer patients.
Ramos, R. N.; Missolo-Koussou, Y.; Gerber-Ferder, Y.; Bromley, C.; Bugatti, M.; Nunez, N. G.; Boari Tosello, J.; Richer, W.; Denizeau, J.; Sedlik, C.; Caudana, P.; Kotsias, F.; Niborski, L. L.; Viel, S.; Bohec, M.; Lameiras, S.; Baulande, S.; Lesage, L.; Nicolas, A.; Meseure, D.; Vincent-Salomon, A.; Reyal, F.; Dutertre, C.-A.; Ginhoux, F.; Vimeux, L.; Donnadieu, E.; Buttard, B.; Galon, J.; Zelenay, S.; Vermi, W.; Guermonprez, P.; Piaggio, E.; Helft, J.
Show abstract
Macrophage infiltration is a hallmark of solid cancers and overall macrophage infiltration is correlated with lower patient survival and resistance to therapy. However, tumor-associated macrophages are phenotypically and functionally heterogeneous. Specific tumor-associated macrophage subsets might be endowed with antagonistic role on cancer progression and on the development of anti-tumor immunity. For instance, monocyte-derived TREM2+ tumor-associated macrophages have pro-tumorigenic and immunosuppressive functions. Here, we identify a discrete population of FOLR2+ tumor-associated macrophages positively correlating with patient survival in breast cancer. FOLR2+ macrophages are evolutionarily conserved across species and populate human and murine healthy mammary gland. Moreover, FOLR2+ macrophages co-localize with lymphoid aggregates containing CD8+ T cells in breast cancer and across ten other types of cancers. This study highlights antagonistic roles for tumor-associated macrophage subsets and paves the way for subset-specific therapeutic interventions in macrophages-based cancer therapies.
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