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. 2015 Apr 2;4(9):e1027473. doi: 10.1080/2162402X.2015.1027473

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© 2015 The Author(s). Published with license by Taylor & Francis Group, LLC

© Serena Lunardi, Su Yin Lim, Ruth J Muschel, and Thomas B Brunner

This is an Open Access article distributed under the terms of the Creative Commons Attribution-Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The moral rights of the named author(s) have been asserted.

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Figure 1. — IP-10 recruits immunosuppressive CXCR3⁺FoxP3⁺ regulatory T cells in pancreatic ductal adenocarcinoma. Pancreatic cancer cells (PCCs) induce pancreatic stellate cells (PSCs) to secrete IP-10 by a yet to be characterized mechanism. IP-10 recruits CXCR3 (the cognate receptor)-expressing CD4⁺/CD8⁺ effector T cells and FoxP3⁺ regulatory T cells (Tregs). However, because circulating Treg numbers are highly elevated relative to effector T cells, CXCR3⁺ Tregs may be preferentially recruited to inhibit adaptive immune responses (via effector T cell, NK cell and APC inhibition), thus contributing to an immunosuppressive and tumor-promoting microenvironment.