<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Chen Y</submitter><funding>Shanghai Songjiang District Research Foundation</funding><funding>Basic and Applied Basic Research Foundation of Guangdong Province</funding><funding>National Natural Science Foundation of China</funding><pagination>21</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12933926</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>33(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Autoimmune inflammation results from dysregulated immune responses, with dysfunction of regulatory T cells (Tregs) being a key contributor due to their critical role in maintaining immune tolerance. The stability and function of Tregs are strongly influenced by the inflammatory microenvironment, yet the regulatory interactions between CD8&lt;sup>+&lt;/sup> T cells and CD4&lt;sup>+&lt;/sup>Foxp3&lt;sup>+&lt;/sup> Tregs remain poorly understood.&lt;h4>Methods&lt;/h4>We investigated the role of CD8&lt;sup>+&lt;/sup> T cells in regulating induced Tregs (iTregs) using in vitro T cell co-culture assays and two in vivo models of autoimmune disease. A naïve CD4&lt;sup>+&lt;/sup> T cell transfer colitis model was used to evaluate the suppressive function of iTregs in the presence or absence of CD8&lt;sup>+&lt;/sup> T cel</pubmed_abstract><journal>Journal of biomedical science</journal><pubmed_title>TGF-β signaling mediates crosstalk between CD8&amp;lt;sup&amp;gt;+&amp;lt;/sup&amp;gt; T cells and CD39&amp;lt;sup&amp;gt;+&amp;lt;/sup&amp;gt; induced Treg cells in autoimmune inflammation.</pubmed_title><pmcid>PMC12933926</pmcid><funding_grant_id>82371817</funding_grant_id><funding_grant_id>82001727</funding_grant_id><funding_grant_id>2024SJKJGG059</funding_grant_id><funding_grant_id>2022A1515111173</funding_grant_id><funding_grant_id>81871224</funding_grant_id><funding_grant_id>2024SJKJGG076</funding_grant_id><pubmed_authors>Liang RZ</pubmed_authors><pubmed_authors>Chen JR</pubmed_authors><pubmed_authors>Liu L</pubmed_authors><pubmed_authors>Lu Y</pubmed_authors><pubmed_authors>Dang JL</pubmed_authors><pubmed_authors>Zhao W</pubmed_authors><pubmed_authors>Xiong YD</pubmed_authors><pubmed_authors>Zheng SG</pubmed_authors><pubmed_authors>Long Q</pubmed_authors><pubmed_authors>Wang J</pubmed_authors><pubmed_authors>Zang N</pubmed_authors><pubmed_authors>Yang Y</pubmed_authors><pubmed_authors>Olsen N</pubmed_authors><pubmed_authors>Chen Y</pubmed_authors><pubmed_authors>Zhao J</pubmed_authors><pubmed_authors>Pan YF</pubmed_authors></additional><is_claimable>false</is_claimable><name>TGF-β signaling mediates crosstalk between CD8&amp;lt;sup&amp;gt;+&amp;lt;/sup&amp;gt; T cells and CD39&amp;lt;sup&amp;gt;+&amp;lt;/sup&amp;gt; induced Treg cells in autoimmune inflammation.</name><description>&lt;h4>Background&lt;/h4>Autoimmune inflammation results from dysregulated immune responses, with dysfunction of regulatory T cells (Tregs) being a key contributor due to their critical role in maintaining immune tolerance. The stability and function of Tregs are strongly influenced by the inflammatory microenvironment, yet the regulatory interactions between CD8&lt;sup>+&lt;/sup> T cells and CD4&lt;sup>+&lt;/sup>Foxp3&lt;sup>+&lt;/sup> Tregs remain poorly understood.&lt;h4>Methods&lt;/h4>We investigated the role of CD8&lt;sup>+&lt;/sup> T cells in regulating induced Tregs (iTregs) using in vitro T cell co-culture assays and two in vivo models of autoimmune disease. A naïve CD4&lt;sup>+&lt;/sup> T cell transfer colitis model was used to evaluate the suppressive function of iTregs in the presence or absence of CD8&lt;sup>+&lt;/sup> T cel</description><dates><release>2026-01-01T00:00:00Z</release><publication>2026 Feb</publication><modification>2026-07-16T20:49:36.639Z</modification><creation>2026-07-10T03:12:05.327Z</creation></dates><accession>S-EPMC12933926</accession><cross_references><pubmed>41736071</pubmed><doi>10.1186/s12929-026-01228-z</doi></cross_references></HashMap>