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OncoImmunology Volume 4, 2015 - Issue 9
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IP-10/CXCL10 attracts regulatory T cells: Implication for pancreatic cancer

Serena LunardiGray Institute for Radiation Oncology and Biology; Department of Oncology; University of Oxford; Oxford, UKCorrespondence[email protected]
,
Su Yin LimGray Institute for Radiation Oncology and Biology; Department of Oncology; University of Oxford; Oxford, UK
,
Ruth J MuschelGray Institute for Radiation Oncology and Biology; Department of Oncology; University of Oxford; Oxford, UK; These authors contributed equally to this work.
&
Thomas B BrunnerGray Institute for Radiation Oncology and Biology; Department of Oncology; University of Oxford; Oxford, UK;Department of Radiation Oncology; University Hospitals Freiburg; Freiburg, Germany; These authors contributed equally to this work.
Article: e1027473 | Received 03 Mar 2015, Accepted 03 Mar 2015, Published online: 27 Jul 2015

Figures & data

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.

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.

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