<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Lin Z</submitter><funding>Natural Science Fund of Jiangsu Province</funding><funding>Social development fund of Yangzhou municipality</funding><funding>National Natural Science Foundation of China</funding><funding>Collaborative Fund of Yangzhou University and Yangzhou municipality</funding><pagination>1159-1173</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11028319</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>67(7)</volume><pubmed_abstract>Regulatory T cells play critical roles in self-tolerance and tumor evasion. CD4&lt;sup>+&lt;/sup>NKG2D&lt;sup>+&lt;/sup> cells with regulatory activity are present in patients with NKG2DL&lt;sup>+&lt;/sup> tumors and juvenile systemic lupus erythematosus. We previously showed that TGF-β-producing CD4&lt;sup>+&lt;/sup>NKG2D&lt;sup>+&lt;/sup> T cells are present in pCD86-Rae-1ε transgenic mice. Here, we performed both ex vivo and in vivo studies on pCD86-Rae-1ε transgenic mice and an MC38 tumor-bearing mouse model and show that NK1.1&lt;sup>-&lt;/sup>CD4&lt;sup>+&lt;/sup>NKG2D&lt;sup>+&lt;/sup> T cells have regulatory activity in pCD86-Rae-1ε transgenic mice. Furthermore, this T-cell subset was induced in mice transplanted with NKG2DL&lt;sup>+&lt;/sup> tumor cells and produced TGF-β and FasL, and secreted low amounts of IFN-γ. This T-cell subse</pubmed_abstract><journal>Cancer immunology, immunotherapy : CII</journal><pubmed_title>Regulatory NK1.1&lt;sup>-&lt;/sup>CD4&lt;sup>+&lt;/sup>NKG2D&lt;sup>+&lt;/sup> subset induced by NKG2DL&lt;sup>+&lt;/sup> cells promotes tumor evasion in mice.</pubmed_title><pmcid>PMC11028319</pmcid><funding_grant_id>81273214</funding_grant_id><funding_grant_id>BK2011449</funding_grant_id><funding_grant_id>81671547</funding_grant_id><funding_grant_id>2012038-5</funding_grant_id><funding_grant_id>BK2008215</funding_grant_id><funding_grant_id>81172785</funding_grant_id><funding_grant_id>81471547</funding_grant_id><funding_grant_id>YZ2014179</funding_grant_id><pubmed_authors>Qian X</pubmed_authors><pubmed_authors>Hu C</pubmed_authors><pubmed_authors>Ding Y</pubmed_authors><pubmed_authors>Zhang Y</pubmed_authors><pubmed_authors>Xiao W</pubmed_authors><pubmed_authors>Jia X</pubmed_authors><pubmed_authors>Lin Z</pubmed_authors><pubmed_authors>Zhu G</pubmed_authors><pubmed_authors>Han S</pubmed_authors><pubmed_authors>Qian L</pubmed_authors><pubmed_authors>Gong W</pubmed_authors></additional><is_claimable>false</is_claimable><name>Regulatory NK1.1&lt;sup>-&lt;/sup>CD4&lt;sup>+&lt;/sup>NKG2D&lt;sup>+&lt;/sup> subset induced by NKG2DL&lt;sup>+&lt;/sup> cells promotes tumor evasion in mice.</name><description>Regulatory T cells play critical roles in self-tolerance and tumor evasion. CD4&lt;sup>+&lt;/sup>NKG2D&lt;sup>+&lt;/sup> cells with regulatory activity are present in patients with NKG2DL&lt;sup>+&lt;/sup> tumors and juvenile systemic lupus erythematosus. We previously showed that TGF-β-producing CD4&lt;sup>+&lt;/sup>NKG2D&lt;sup>+&lt;/sup> T cells are present in pCD86-Rae-1ε transgenic mice. Here, we performed both ex vivo and in vivo studies on pCD86-Rae-1ε transgenic mice and an MC38 tumor-bearing mouse model and show that NK1.1&lt;sup>-&lt;/sup>CD4&lt;sup>+&lt;/sup>NKG2D&lt;sup>+&lt;/sup> T cells have regulatory activity in pCD86-Rae-1ε transgenic mice. Furthermore, this T-cell subset was induced in mice transplanted with NKG2DL&lt;sup>+&lt;/sup> tumor cells and produced TGF-β and FasL, and secreted low amounts of IFN-γ. This T-cell subse</description><dates><release>2018-01-01T00:00:00Z</release><publication>2018 Jul</publication><modification>2025-04-22T20:40:31.833Z</modification><creation>2025-04-06T03:17:03.529Z</creation></dates><accession>S-EPMC11028319</accession><cross_references><pubmed>29802426</pubmed><doi>10.1007/s00262-018-2172-6</doi></cross_references></HashMap>