<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Almohammad K</submitter><funding>SFB1506: "Aging at Interfaces" to H.J. and J.T.</funding><funding>CRC1279 : "Exploiting the Human Peptidome for Novel Antimicrobial and Anticancer Agents" to H.J.</funding><funding>S.V.</funding><funding>H.J.</funding><funding>Further project funding by the DFG was granted to S.V. and F.G.</funding><funding>J.T.</funding><pagination>e70137</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12832068</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>56(1)</volume><pubmed_abstract>Glucocorticoids (GCs) regulate diverse physiological processes, comprising metabolism, immune responses, stress adaptation, and inflammation. Synthetic GCs are widely used for their powerful anti-inflammatory and immunosuppressive effects, in the treatment of autoimmune diseases, allergies, and inflammation. Here, we investigated the role of the glucocorticoid receptor (GR) in B cell development and survival using both B cell-specific GR-deficient mice and continuous in vivo GR agonist treatments. Deletion of the GR in B cells altered splenic B cell subpopulations, increasing follicular and CD21&lt;sup>lo&lt;/sup> B cells and leading to the accumulation of IgM&lt;sup>-&lt;/sup>/IgD&lt;sup>-&lt;/sup> B cells. In vivo treatment with GR agonists, such as Dexamethasone (Dex) and Prednisolone (Pred), selectively</pubmed_abstract><journal>European journal of immunology</journal><pubmed_title>IgD-Expressing Mature B Cells Exhibit Enhanced Sensitivity to Glucocorticoid-Induced Cell Death.</pubmed_title><pmcid>PMC12832068</pmcid><funding_grant_id>505870049</funding_grant_id><funding_grant_id>B03</funding_grant_id><funding_grant_id>497680553</funding_grant_id><funding_grant_id>B05</funding_grant_id><funding_grant_id>450627322</funding_grant_id><funding_grant_id>C05</funding_grant_id><funding_grant_id>326914434</funding_grant_id><funding_grant_id>537908488</funding_grant_id><pubmed_authors>Setz CS</pubmed_authors><pubmed_authors>Alkhatib M</pubmed_authors><pubmed_authors>Almohammad K</pubmed_authors><pubmed_authors>Greulich F</pubmed_authors><pubmed_authors>Jumaa H</pubmed_authors><pubmed_authors>Tuckermann J</pubmed_authors><pubmed_authors>Young M</pubmed_authors><pubmed_authors>Vettorazzi S</pubmed_authors></additional><is_claimable>false</is_claimable><name>IgD-Expressing Mature B Cells Exhibit Enhanced Sensitivity to Glucocorticoid-Induced Cell Death.</name><description>Glucocorticoids (GCs) regulate diverse physiological processes, comprising metabolism, immune responses, stress adaptation, and inflammation. Synthetic GCs are widely used for their powerful anti-inflammatory and immunosuppressive effects, in the treatment of autoimmune diseases, allergies, and inflammation. Here, we investigated the role of the glucocorticoid receptor (GR) in B cell development and survival using both B cell-specific GR-deficient mice and continuous in vivo GR agonist treatments. Deletion of the GR in B cells altered splenic B cell subpopulations, increasing follicular and CD21&lt;sup>lo&lt;/sup> B cells and leading to the accumulation of IgM&lt;sup>-&lt;/sup>/IgD&lt;sup>-&lt;/sup> B cells. In vivo treatment with GR agonists, such as Dexamethasone (Dex) and Prednisolone (Pred), selectively</description><dates><release>2026-01-01T00:00:00Z</release><publication>2026 Jan</publication><modification>2026-06-06T22:26:09.231Z</modification><creation>2026-06-06T03:07:53.88Z</creation></dates><accession>S-EPMC12832068</accession><cross_references><pubmed>41581071</pubmed><doi>10.1002/eji.70137</doi></cross_references></HashMap>