Undisclosed CLEC-1 mAbs

Moreover, the synergy with chemotherapy treatment (cyclophosphamide, gemcitabine) in the MC38 model of colon adenocarcinoma in Clec1a deficient animals significantly enhanced complete responses. Mechanistically, the in vivo phagocytosis of tumor cells (Hepa1.6 and MCA101) by macrophages was enhanced in CLEC-1 deficient animals compared to WT animals. Altogether, our results demonstrate that CLEC-1 acts as a novel immune checkpoint in myeloid cells and highlight its high potential as a target for innovative immunotherapy in oncology.

Antagonist anti-CLEC-1 or anti-TRIM21 antibodies are therefore being evaluated to further confirm the involvement of the newly identified CLEC-1 interaction with TRIM21 in the regulation of CLEC-1’s function as an inhibitory myeloid checkpoint. Altogether our data highlight the CLEC-1/TRIM21 axis as a new target for cancer immunotherapy.