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. 2019 May 9;10:1014. doi: 10.3389/fimmu.2019.01014

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Copyright © 2019 Noubade, Majri-Morrison and Tarbell.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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An integrated model of DC crosstalk for anti-tumor immunity. Outline of the multicellular orchestration of events that can contribute to a robust anti-tumor response. (Note: not all events happen in every context, and the order may also differ). (1) Intratumoral migratory-cDC1 and -cDC2s scavenge tumor-derived antigens and migrate to tumor dLN. (2) migratory-cDC2s (mig-cDC2) present MHC class II-restricted tumor antigen to CD4 T cells and induce expression of molecules such as CD40L (3) Migratory-cDC1s (mig-cDC1) prime and activate naïve CD8 T cells; (4) these activated CD8 T cells produce XCL1 and CCL3/4 to draw in XCR1+LN-resident-cDC1s and CCR5+ pDCs to the site of initial priming. (5) Mig-cDC1s can hand-off antigen to the newly recruited, LN-resident-cDC1. (6) pDCs produce type I IFN to mature cDCs. (7) The licensed CTL with enhanced effector functions undergoes clonal expansion and moves to the tumor to induce tumor cell killing. (8) The activated CD8 T cells and NK cells can mediate further increase in cDC1 numbers by producing XCL1 and FLT3L.