<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>25(10)</volume><submitter>Gefen T</submitter><funding>Sylvester Comprehensive Cancer Center, Medical School, University of Miami</funding><funding>Dodson Interdisciplinary Immunotherapy Institute</funding><pubmed_abstract>T cell immunoglobulin-3 (TIM-3) is a negative regulator of interferon-γ (IFN-γ) secreting CD4&lt;sup>+&lt;/sup> T cells and CD8&lt;sup>+&lt;/sup> T cytotoxic cells. Recent studies have highlighted the role of TIM-3 as an important mediator of CD8&lt;sup>+&lt;/sup> T cell exhaustion in the setting of chronic viral infections and cancer. In murine tumor models, antibody blockade of TIM-3 with anti-TIM-3 antibodies as monotherapy has no or minimal antitumor activity, suggesting that TIM-3 signaling exerts an accessory or amplifying effect in keeping immune responses in check. Using a combined bead and cell-based systemic evolution of ligands by exponential enrichment (SELEX) protocol, we have isolated nuclease-resistant oligonucleotide aptamer ligands that bind to cell-associated TIM-3 with high affinity and s</pubmed_abstract><journal>Molecular therapy : the journal of the American Society of Gene Therapy</journal><pagination>2280-2288</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5628791</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>A TIM-3 Oligonucleotide Aptamer Enhances T Cell Functions and Potentiates Tumor Immunity in Mice.</pubmed_title><pmcid>PMC5628791</pmcid><pubmed_authors>Puplampu-Dove Y</pubmed_authors><pubmed_authors>Gefen T</pubmed_authors><pubmed_authors>Castro I</pubmed_authors><pubmed_authors>Patel S</pubmed_authors><pubmed_authors>Gilboa E</pubmed_authors><pubmed_authors>Muharemagic D</pubmed_authors></additional><is_claimable>false</is_claimable><name>A TIM-3 Oligonucleotide Aptamer Enhances T Cell Functions and Potentiates Tumor Immunity in Mice.</name><description>T cell immunoglobulin-3 (TIM-3) is a negative regulator of interferon-γ (IFN-γ) secreting CD4&lt;sup>+&lt;/sup> T cells and CD8&lt;sup>+&lt;/sup> T cytotoxic cells. Recent studies have highlighted the role of TIM-3 as an important mediator of CD8&lt;sup>+&lt;/sup> T cell exhaustion in the setting of chronic viral infections and cancer. In murine tumor models, antibody blockade of TIM-3 with anti-TIM-3 antibodies as monotherapy has no or minimal antitumor activity, suggesting that TIM-3 signaling exerts an accessory or amplifying effect in keeping immune responses in check. Using a combined bead and cell-based systemic evolution of ligands by exponential enrichment (SELEX) protocol, we have isolated nuclease-resistant oligonucleotide aptamer ligands that bind to cell-associated TIM-3 with high affinity and s</description><dates><release>2017-01-01T00:00:00Z</release><publication>2017 Oct</publication><modification>2025-04-20T03:39:13.921Z</modification><creation>2019-03-26T23:57:55Z</creation></dates><accession>S-EPMC5628791</accession><cross_references><pubmed>28800954</pubmed><doi>10.1016/j.ymthe.2017.06.023</doi></cross_references></HashMap>