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IL-2 therapy promotes suppressive ICOS+ Treg expansion in melanoma patients
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IL-2 therapy promotes suppressive ICOS+ Treg expansion in melanoma patients
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Journal Article
IL-2 therapy promotes suppressive ICOS+ Treg expansion in melanoma patients
2014
Overview
High-dose (HD) IL-2 therapy in patients with cancer increases the general population of Tregs, which are positive for CD4, CD25, and the Treg-specific marker Foxp3. It is unknown whether specific subsets of Tregs are activated and expanded during HD IL-2 therapy or whether activation of any particular Treg subset correlates with clinical outcome. Here, we evaluated Treg population subsets that were induced in patients with melanoma following HD IL-2 therapy. We identified a Treg population that was positive for CD4, CD25, Foxp3, and the inducible T cell costimulator (ICOS). This Treg population increased more than any other lymphocyte subset during HD IL-2 therapy and had an activated Treg phenotype, as indicated by high levels of CD39, CD73, and TGF-β. ICOS(+) Tregs were the most proliferative lymphocyte population in the blood after IL-2 therapy. Patients with melanoma with enhanced expansion of ICOS(+) Tregs in blood following the first cycle of HD IL-2 therapy had worse clinical outcomes than patients with fewer ICOS(+) Tregs. However, there was no difference in total Treg expansion between HD IL-2 responders and nonresponders. These data suggest that increased expansion of the ICOS(+) Treg population following the first cycle of HD IL-2 therapy may be predictive of clinical outcome.
Publisher
American Society for Clinical Investigation
Subject
/ Antineoplastic Agents - administration & dosage
/ Antineoplastic Agents - pharmacology
/ Cell Proliferation - drug effects
/ Female
/ Humans
/ Inducible T-Cell Co-Stimulator Protein - metabolism
/ Interleukin-2 - administration & dosage
/ Interleukin-2 - pharmacology
/ Male
/ Receptors, Antigen, T-Cell - metabolism
/ T-Lymphocyte Subsets - drug effects
/ T-Lymphocyte Subsets - physiology
/ T-Lymphocytes, Regulatory - drug effects
