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oai:repisalud.isciii.es:20.500.12105/272602026-02-23T01:16:03Zcom_20.500.12105_2273com_20.500.12105_2202col_20.500.12105_19571

00925njm 22002777a 4500 dc Salmon, Hélène author Idoyaga, Juliana author Rahman, Adeeb author Leboeuf, Marylène author Remark, Romain author Jordan, Stefan author Casanova-Acebes, Maria author Khudoynazarova, Makhzuna author Agudo, Judith author Tung, Navpreet author Chakarov, Svetoslav author Rivera, Christina author Hogstad, Brandon author Bosenberg, Marcus author Hashimoto, Daigo author Gnjatic, Sacha author Bhardwaj, Nina author Palucka, Anna Karolina author Brown, Brian D author Brody, Joshua author Ginhoux, Florent author Merad, Miriam author 2016-04-19 Large numbers of melanoma lesions develop resistance to targeted inhibition of mutant BRAF or fail to respond to checkpoint blockade. We explored whether modulation of intratumoral antigen-presenting cells (APCs) could increase responses to these therapies. Using mouse melanoma models, we found that CD103(+) dendritic cells (DCs) were the only APCs transporting intact antigens to the lymph nodes and priming tumor-specific CD8(+) T cells. CD103(+) DCs were required to promote anti-tumoral effects upon blockade of the checkpoint ligand PD-L1; however, PD-L1 inhibition only led to partial responses. Systemic administration of the growth factor FLT3L followed by intratumoral poly I:C injections expanded and activated CD103(+) DC progenitors in the tumor, enhancing responses to BRAF and PD-L1 blockade and protecting mice from tumor rechallenge. Thus, the paucity of activated CD103(+) DCs in tumors limits checkpoint-blockade efficacy and combined FLT3L and poly I:C therapy can enhance tumor responses to checkpoint and BRAF blockade. Immunity . 2016 Apr 19;44(4):924-38. https://hdl.handle.net/20.500.12105/27260 27096321 Immunity ANTITUMOR IMMUNITY METASTATIC MELANOMA CANCER-THERAPY BONE-MARROW IN-VIVO REVEALS LINEAGE STRATEGIES TOLERANCE OCTOGENY Expansion and Activation of CD103(+) Dendritic Cell Progenitors at the Tumor Site Enhances Tumor Responses to Therapeutic PD-L1 and BRAF Inhibition.