<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Dar AA</submitter><funding>NICHD NIH HHS</funding><funding>NIAID NIH HHS</funding><funding>HHS | NIH | National Institute of Allergy and Infectious Diseases</funding><funding>NCI NIH HHS</funding><pagination>982-991</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11060073</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>212(6)</volume><pubmed_abstract>Multiple sclerosis, and its murine model experimental autoimmune encephalomyelitis (EAE), is a neurodegenerative autoimmune disease of the CNS characterized by T cell influx and demyelination. Similar to other autoimmune diseases, therapies can alleviate symptoms but often come with side effects, necessitating the exploration of new treatments. We recently demonstrated that the Cullin-RING E3 ubiquitin ligase 4b (CRL4b) aided in maintaining genome stability in proliferating T cells. In this study, we examined whether CRL4b was required for T cells to expand and drive EAE. Mice lacking Cul4b (Cullin 4b) in T cells had reduced EAE symptoms and decreased inflammation during the peak of the disease. Significantly fewer CD4+ and CD8+ T cells were found in the CNS, particularly among the CD4+ T </pubmed_abstract><journal>Journal of immunology (Baltimore, Md. : 1950)</journal><pubmed_title>CRL4b Inhibition Ameliorates Experimental Autoimmune Encephalomyelitis Progression.</pubmed_title><pmcid>PMC11060073</pmcid><funding_grant_id>R01 AI148240</funding_grant_id><funding_grant_id>R01 CA251425</funding_grant_id><funding_grant_id>T32 HD083185</funding_grant_id><pubmed_authors>Wu K</pubmed_authors><pubmed_authors>Porter N</pubmed_authors><pubmed_authors>Ortega Y</pubmed_authors><pubmed_authors>Aktas S</pubmed_authors><pubmed_authors>Pan ZQ</pubmed_authors><pubmed_authors>Guha I</pubmed_authors><pubmed_authors>Oliver PM</pubmed_authors><pubmed_authors>Dar AA</pubmed_authors><pubmed_authors>Rosen S</pubmed_authors><pubmed_authors>DeVita RJ</pubmed_authors></additional><is_claimable>false</is_claimable><name>CRL4b Inhibition Ameliorates Experimental Autoimmune Encephalomyelitis Progression.</name><description>Multiple sclerosis, and its murine model experimental autoimmune encephalomyelitis (EAE), is a neurodegenerative autoimmune disease of the CNS characterized by T cell influx and demyelination. Similar to other autoimmune diseases, therapies can alleviate symptoms but often come with side effects, necessitating the exploration of new treatments. We recently demonstrated that the Cullin-RING E3 ubiquitin ligase 4b (CRL4b) aided in maintaining genome stability in proliferating T cells. In this study, we examined whether CRL4b was required for T cells to expand and drive EAE. Mice lacking Cul4b (Cullin 4b) in T cells had reduced EAE symptoms and decreased inflammation during the peak of the disease. Significantly fewer CD4+ and CD8+ T cells were found in the CNS, particularly among the CD4+ T </description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Mar</publication><modification>2025-04-03T23:56:49.963Z</modification><creation>2025-04-03T23:56:49.963Z</creation></dates><accession>S-EPMC11060073</accession><cross_references><pubmed>38265261</pubmed><doi>10.4049/jimmunol.2300754</doi></cross_references></HashMap>