<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Dhaeze T</submitter><funding>CIHR</funding><pagination>652-665</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6804668</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>16(7)</volume><pubmed_abstract>CD70 is the unique ligand of CD27 and is expressed on immune cells only upon activation. Therefore, engagement of the costimulatory CD27/CD70 pathway is solely dependent on upregulation of CD70. However, the T cell-intrinsic effect and function of human CD70 remain underexplored. Herein, we describe that CD70 expression distinguishes proinflammatory CD4&lt;sup>+&lt;/sup> T lymphocytes that display an increased potential to migrate into the central nervous system (CNS). Upregulation of CD70 on CD4&lt;sup>+&lt;/sup> T lymphocytes is induced by TGF-β1 and TGF-β3, which promote a pathogenic phenotype. In addition, CD70 is associated with a T&lt;sub>H&lt;/sub>1 and T&lt;sub>H&lt;/sub>17 profile of lymphocytes and is important for T-bet and IFN-γ expression by both T helper subtypes. Moreover, adoptive transfer of CD70</pubmed_abstract><journal>Cellular &amp; molecular immunology</journal><pubmed_title>CD70 defines a subset of proinflammatory and CNS-pathogenic T&lt;sub>H&lt;/sub>1/T&lt;sub>H&lt;/sub>17 lymphocytes and is overexpressed in multiple sclerosis.</pubmed_title><pmcid>PMC6804668</pmcid><funding_grant_id>PJI-153195</funding_grant_id><funding_grant_id>MOP 89885</funding_grant_id><pubmed_authors>Dhaeze T</pubmed_authors><pubmed_authors>Ayrignac X</pubmed_authors><pubmed_authors>Prat A</pubmed_authors><pubmed_authors>Peelen E</pubmed_authors><pubmed_authors>Grasmuck C</pubmed_authors><pubmed_authors>Larochelle C</pubmed_authors><pubmed_authors>Girard M</pubmed_authors><pubmed_authors>Moumdjian R</pubmed_authors><pubmed_authors>Rebillard RM</pubmed_authors><pubmed_authors>Poirier J</pubmed_authors><pubmed_authors>Lahav B</pubmed_authors><pubmed_authors>Bouthillier A</pubmed_authors><pubmed_authors>Larouche S</pubmed_authors><pubmed_authors>Lachance C</pubmed_authors><pubmed_authors>Zandee S</pubmed_authors><pubmed_authors>Duquette P</pubmed_authors><pubmed_authors>Bourbonniere L</pubmed_authors><pubmed_authors>Tremblay L</pubmed_authors></additional><is_claimable>false</is_claimable><name>CD70 defines a subset of proinflammatory and CNS-pathogenic T&lt;sub>H&lt;/sub>1/T&lt;sub>H&lt;/sub>17 lymphocytes and is overexpressed in multiple sclerosis.</name><description>CD70 is the unique ligand of CD27 and is expressed on immune cells only upon activation. Therefore, engagement of the costimulatory CD27/CD70 pathway is solely dependent on upregulation of CD70. However, the T cell-intrinsic effect and function of human CD70 remain underexplored. Herein, we describe that CD70 expression distinguishes proinflammatory CD4&lt;sup>+&lt;/sup> T lymphocytes that display an increased potential to migrate into the central nervous system (CNS). Upregulation of CD70 on CD4&lt;sup>+&lt;/sup> T lymphocytes is induced by TGF-β1 and TGF-β3, which promote a pathogenic phenotype. In addition, CD70 is associated with a T&lt;sub>H&lt;/sub>1 and T&lt;sub>H&lt;/sub>17 profile of lymphocytes and is important for T-bet and IFN-γ expression by both T helper subtypes. Moreover, adoptive transfer of CD70</description><dates><release>2019-01-01T00:00:00Z</release><publication>2019 Jul</publication><modification>2025-04-19T03:38:11.258Z</modification><creation>2020-07-04T07:18:36Z</creation></dates><accession>S-EPMC6804668</accession><cross_references><pubmed>30635649</pubmed><doi>10.1038/s41423-018-0198-5</doi></cross_references></HashMap>