<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>17(1)</volume><submitter>Conde E</submitter><pubmed_abstract>IL-33 is an inflammatory cytokine contributing to asthma, Chronic Obstructive Pulmonary Disease (COPD), and autoimmune diseases. Although recent studies suggest that IL-33 can induce the generation of autoantibodies, the role of IL-33 on B cell maturation and tolerance is poorly understood. Here, by inducing systemic overexpression of IL-33 in mice, we show that this cytokine induces the IL-5 and CD4 T cell-dependent accumulation of plasmablasts and plasma cells of all isotypes in the spleen, and leads to an increased antibody production. IL-33 also disrupts splenic architecture and elevates autoantibody production, indicating a break in peripheral tolerance. Consistently, elevated levels of IL-33 exacerbate autoantibody production, kidney damage, and decrease survival in a mouse model of </pubmed_abstract><journal>Nature communications</journal><pagination>1102</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12852098</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>IL-33 expands plasma cells, disrupts germinal centers, and increases autoantibody production in mice.</pubmed_title><pmcid>PMC12852098</pmcid><pubmed_authors>Conde E</pubmed_authors><pubmed_authors>Asrat S</pubmed_authors><pubmed_authors>Orengo JM</pubmed_authors><pubmed_authors>Gayvert K</pubmed_authors><pubmed_authors>Yarilin D</pubmed_authors><pubmed_authors>Murphy AJ</pubmed_authors><pubmed_authors>Vecchione A</pubmed_authors><pubmed_authors>Limnander A</pubmed_authors><pubmed_authors>Lim WK</pubmed_authors><pubmed_authors>Ben LH</pubmed_authors><pubmed_authors>Huang S</pubmed_authors><pubmed_authors>Birchard D</pubmed_authors><pubmed_authors>Pedraza P</pubmed_authors><pubmed_authors>Sleeman MA</pubmed_authors><pubmed_authors>Tasker C</pubmed_authors></additional><is_claimable>false</is_claimable><name>IL-33 expands plasma cells, disrupts germinal centers, and increases autoantibody production in mice.</name><description>IL-33 is an inflammatory cytokine contributing to asthma, Chronic Obstructive Pulmonary Disease (COPD), and autoimmune diseases. Although recent studies suggest that IL-33 can induce the generation of autoantibodies, the role of IL-33 on B cell maturation and tolerance is poorly understood. Here, by inducing systemic overexpression of IL-33 in mice, we show that this cytokine induces the IL-5 and CD4 T cell-dependent accumulation of plasmablasts and plasma cells of all isotypes in the spleen, and leads to an increased antibody production. IL-33 also disrupts splenic architecture and elevates autoantibody production, indicating a break in peripheral tolerance. Consistently, elevated levels of IL-33 exacerbate autoantibody production, kidney damage, and decrease survival in a mouse model of </description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Dec</publication><modification>2026-06-16T07:11:45.106Z</modification><creation>2026-06-16T03:09:46.712Z</creation></dates><accession>S-EPMC12852098</accession><cross_references><pubmed>41436488</pubmed><doi>10.1038/s41467-025-67867-2</doi></cross_references></HashMap>