<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>13</volume><submitter>Xia CQ</submitter><pubmed_abstract>&lt;h4>Background&lt;/h4>ATG has been employed to deplete T cells in several immune-mediated conditions. However, whether ATG administration affects naïve and memory T cell differently is largely unknown. THE CONTEXT AND PURPOSE OF THE STUDY: In this study, we assessed how murine ATG therapy affected T cell subsets in NOD mice, based on their regulatory and naïve or memory phenotype, as well as its influence on antigen-specific immune responses.&lt;h4>Results&lt;/h4>Peripheral blood CD4+ and CD8+ T cells post-ATG therapy declined to their lowest levels at day 3, while CD4+ T cells returned to normal levels more rapidly than CD8+ T cells. ATG therapy failed to eliminate antigen-primed T cells. CD4+ T cell responses post-ATG therapy skewed to T helper type 2 (Th2) and possibly IL-10-producing T regulatory type 1 (Tr1) cells. Intriguingly, Foxp3+ regulatory T cells (Tregs) were less sensitive to ATG depletion and remained at higher levels following in vivo recovery compared to controls. Of note, the frequency of Foxp3+ Tregs with memory T cell phenotype was significantly increased in ATG-treated animals.&lt;h4>Conclusion&lt;/h4>ATG therapy may modulate antigen-specific immune responses through inducing memory-like regulatory T cells as well as other protective T cells such as Th2 and IL-10-producing Tr1 cells.</pubmed_abstract><journal>BMC immunology</journal><pagination>70</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3547787</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Anti-thymocyte globulin (ATG) differentially depletes naive and memory T cells and permits memory-type regulatory T cells in nonobese diabetic mice.</pubmed_title><pmcid>PMC3547787</pmcid><pubmed_authors>Xia CQ</pubmed_authors><pubmed_authors>Wan S</pubmed_authors><pubmed_authors>Looney BM</pubmed_authors><pubmed_authors>Williams J</pubmed_authors><pubmed_authors>Wasserfall CH</pubmed_authors><pubmed_authors>Atkinson MA</pubmed_authors><pubmed_authors>Eisenbeis S</pubmed_authors><pubmed_authors>Chernatynskaya AV</pubmed_authors><pubmed_authors>Clare-Salzler MJ</pubmed_authors></additional><is_claimable>false</is_claimable><name>Anti-thymocyte globulin (ATG) differentially depletes naive and memory T cells and permits memory-type regulatory T cells in nonobese diabetic mice.</name><description>&lt;h4>Background&lt;/h4>ATG has been employed to deplete T cells in several immune-mediated conditions. However, whether ATG administration affects naïve and memory T cell differently is largely unknown. THE CONTEXT AND PURPOSE OF THE STUDY: In this study, we assessed how murine ATG therapy affected T cell subsets in NOD mice, based on their regulatory and naïve or memory phenotype, as well as its influence on antigen-specific immune responses.&lt;h4>Results&lt;/h4>Peripheral blood CD4+ and CD8+ T cells post-ATG therapy declined to their lowest levels at day 3, while CD4+ T cells returned to normal levels more rapidly than CD8+ T cells. ATG therapy failed to eliminate antigen-primed T cells. CD4+ T cell responses post-ATG therapy skewed to T helper type 2 (Th2) and possibly IL-10-producing T regulatory type 1 (Tr1) cells. Intriguingly, Foxp3+ regulatory T cells (Tregs) were less sensitive to ATG depletion and remained at higher levels following in vivo recovery compared to controls. Of note, the frequency of Foxp3+ Tregs with memory T cell phenotype was significantly increased in ATG-treated animals.&lt;h4>Conclusion&lt;/h4>ATG therapy may modulate antigen-specific immune responses through inducing memory-like regulatory T cells as well as other protective T cells such as Th2 and IL-10-producing Tr1 cells.</description><dates><release>2012-01-01T00:00:00Z</release><publication>2012 Dec</publication><modification>2024-10-15T04:41:00.992Z</modification><creation>2019-03-27T01:03:26Z</creation></dates><accession>S-EPMC3547787</accession><cross_references><pubmed>23237483</pubmed><doi>10.1186/1471-2172-13-70</doi></cross_references></HashMap>