Leveraging TNFR2 for antitumour immunity: T reg depletion and myeloid reprogramming versus T cell costimulation
Linda MårtenssoniD, Petra HolmkvistiD, Kirstie L.S. ClearyiD, Carolin SvenssoniD, Monika SemmrichiD, Niyaz YoosufiD, Alexandra Gabriela FerreiraiD, Mathilda KovacekiD, Mimoza BodéniD, Therese BlidbergiD, Osman DadasiD, Jenny MattssoniD, David ErmertiD, Elin BirgerssoniD, Vicentiu Andrei PiticiD, Martin C. TayloriD, Mona YazdaniiD, Ulla‐Carin TornbergiD, Ingrid KarlssoniD, Sean H. LimiD, Stephen A. BeersiD, Mark Steven CraggiD, Björn FrendéusiD, Ingrid TeigeiD
Abstract
Although checkpoint inhibitors have revolutionized cancer treatment, responses are largely restricted to targeting CTLA-4 and PD-(L)1. TNFR2 has been identified as a target of interest, but a lack of understanding of whether agonists or blockers should be used, and whether Fc{gamma}R interactions promote effcacy, has hampered therapeutic antibody development. Here, we engineered two distinct -TNFR2 types: ligand-blocking Fc{gamma}R-engaging versus non-ligand-blocking agonist antibodies. Both showed potent anti-tumor effcacy across multiple syngeneic mouse tumor models and combined effectively with -PD-1. The ligand-blocking antibody depleted intratumoral T regs and reprogrammed the myeloid compartment, directing monocytes towards a pro-inflammatory macrophage and dendritic cell trajectory. Surprisingly, this effect depended on both inhibitory and activating Fc{gamma}Rs. In contrast, the agonist directly co-stimulated T and NK cells, through partially Fc{gamma}R-independent mechanisms. Both antibodies converged on activating tumor-specific CD8+ T cells mediating tumor rejection. Clinical assessment of both ligand-blocking (BI-1808) and agonist (BI-1910) -TNFR2 antibodies is currently ongoing. Graphical abstractO_LILigand-blocking anti-TNFR2 mAbs (BI-1808 and 3F10) deplete CCR8+ T regs and activate myeloid cells, remodeling the TME and leading to CD8+ T cell killing of cancer cells. T reg depletion and myeloid activation are mediated through interaction with activating Fc{gamma}Rs and the inhibitory Fc{gamma}RIIB, respectively. C_LIO_LIAgonist anti-TNFR2 mAbs (BI-1910 and 5A05) intrinsically agonize TNFR2 on T cells and NK cells, which is enhanced by Fc{gamma}RIIB crosslinking. The resulting broad lymphocyte activation mediates cancer cell killing. C_LI O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=127 SRC="FIGDIR/small/697572v1_ufig1.gif" ALT="Figure 1"> View larger version (30K): org.highwire.dtl.DTLVardef@3ecc17org.highwire.dtl.DTLVardef@c936a7org.highwire.dtl.DTLVardef@23189aorg.highwire.dtl.DTLVardef@243a05_HPS_FORMAT_FIGEXP M_FIG C_FIG
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