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               <mods:identifier type="citation">Immunity  . 2016 Apr 19;44(4):924-38.</mods:identifier>
               <mods:identifier type="uri">https://hdl.handle.net/20.500.12105/27260</mods:identifier>
               <mods:identifier type="pubmedID">27096321</mods:identifier>
               <mods:identifier type="journal">Immunity</mods:identifier>
               <mods:abstract>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.</mods:abstract>
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                  <mods:topic>ANTITUMOR IMMUNITY</mods:topic>
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                  <mods:topic>METASTATIC MELANOMA</mods:topic>
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                  <mods:title>Expansion and Activation of CD103(+) Dendritic Cell Progenitors at the Tumor Site Enhances Tumor Responses to Therapeutic PD-L1 and BRAF Inhibition.</mods:title>
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