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Dipeptidylpeptidase 4 inhibition enhances lymphocyte trafficking, improving both naturally occurring tumor immunity and immunotherapy
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Dipeptidylpeptidase 4 inhibition enhances lymphocyte trafficking, improving both naturally occurring tumor immunity and immunotherapy
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Journal Article
Dipeptidylpeptidase 4 inhibition enhances lymphocyte trafficking, improving both naturally occurring tumor immunity and immunotherapy
2015
Overview
Post-translational modification of chemokines such as CXCL10 can regulate their activity. Albert and colleagues demonstrate that the endogenous peptidase DPP4 cleaves CXCL10 and thereby interferes with T cell recruitment to tumors.
The success of antitumor immune responses depends on the infiltration of solid tumors by effector T cells, a process guided by chemokines. Here we show that
in vivo
post-translational processing of chemokines by dipeptidylpeptidase 4 (DPP4, also known as CD26) limits lymphocyte migration to sites of inflammation and tumors. Inhibition of DPP4 enzymatic activity enhanced tumor rejection by preserving biologically active CXCL10 and increasing trafficking into the tumor by lymphocytes expressing the counter-receptor CXCR3. Furthermore, DPP4 inhibition improved adjuvant-based immunotherapy, adoptive T cell transfer and checkpoint blockade. These findings provide direct
in vivo
evidence for control of lymphocyte trafficking via CXCL10 cleavage and support the use of DPP4 inhibitors for stabilizing biologically active forms of chemokines as a strategy to enhance tumor immunotherapy.
Publisher
Nature Publishing Group US,Nature Publishing Group
Subject
/ Animals
/ Cell Movement - drug effects
/ Chemokine CXCL10 - immunology
/ Chemokine CXCL10 - metabolism
/ Dipeptidyl Peptidase 4 - genetics
/ Dipeptidyl Peptidase 4 - immunology
/ Dipeptidyl Peptidase 4 - metabolism
/ Dipeptidyl-Peptidase IV Inhibitors - pharmacology
/ Female
/ Male
/ Neoplasms, Experimental - genetics
/ Neoplasms, Experimental - immunology
/ Neoplasms, Experimental - therapy
/ Receptors, CXCR3 - immunology
/ Receptors, CXCR3 - metabolism
/ Tumors
