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. 2021 Apr 15;11:591386. doi: 10.3389/fonc.2021.591386

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Copyright © 2021 Santagata, Ieranò, Trotta, Capiluongo, Auletta, Guardascione and Scala

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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CXCL12/CXCR4/CXCR7 axis in TME. CXCL12 is responsible for TME suppressive cell populations recruitment. CXCL12 induces vascular permeability and allows tumor cell extravasation, thus promoting the metastatic process. ECs CXCR7-positive promote primary tumor growth through secretion of angiogenic factors, such as VEGF. CXCR4 promotes migration and survival of MDSCs and CXCR7 enhances the infiltration of M-MDSCs. The expression of CXCR4 on Tregs promotes intratumoral migration.. CD8+ T cells express CXCR4. Regulatory B cells are recruited to the tumor by CXCL12/CXCR4 and CXCR7 overexpression is involved in the regulation of B cells development and differentiation. Intratumoral CXCR4+ DCs stimulate cytotoxic T cells. Plasmacytoid DCs express CXCR7.