{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Tan C"],"funding":["Howard Hughes Medical Institute","Burroughs Wellcome Fund","NIAID NIH HHS","Rheumatology Research Foundation","U.S. Department of Health & Human Services | NIH | National Institute of Arthritis and Musculoskeletal and Skin Diseases","Uehara Memorial Foundation","NIAMS NIH HHS","Cancer Research Institute","Chan–Zuckerberg Biohub; Innovative Genomics Institute; Parker Institute for Cancer Immunotherapy","Division of Intramural Research, National Institute of Allergy and Infectious Diseases"],"pagination":["1267-1279"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8081071"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["21(10)"],"pubmed_abstract":["Antigen stimulation (signal 1) triggers B cell proliferation and primes B cells to recruit, engage and respond to T cell help (signal 2). Failure to receive signal 2 within a defined time window results in B cell apoptosis, yet the mechanisms that enforce dependence on co-stimulation are incompletely understood. Nr4a1-3 encode a small family of orphan nuclear receptors that are rapidly induced by B cell antigen receptor stimulation. Here, we show that Nr4a1 and Nr4a3 play partially redundant roles to restrain B cell responses to antigen in the absence of co-stimulation and do so, in part, by repressing the expression of BATF and, consequently, MYC. The NR4A family also restrains B cell access to T cell help by repressing expression of the T cell chemokines CCL3 and CCL4, as well as CD86 an"],"journal":["Nature immunology"],"pubmed_title":["NR4A nuclear receptors restrain B cell responses to antigen when second signals are absent or limiting."],"pmcid":["PMC8081071"],"funding_grant_id":["R01 AR069520","R01AR069520","5T32AI007334-28","HHMI Medical Research Fellows program","Lloyd J. Old STAR grant","Innovative Research Award","Career Award for Medical Scientists","T32 AI007334","R01 AI148487"],"pubmed_authors":["Hiwa R","Brooks JF","Noviski M","Hibiya K","Huizar J","Tan C","Zikherman J","Garcia J","Heyn C","Li Z","Vykunta V","Mueller JL","Marson A"],"additional_accession":[]},"is_claimable":false,"name":"NR4A nuclear receptors restrain B cell responses to antigen when second signals are absent or limiting.","description":"Antigen stimulation (signal 1) triggers B cell proliferation and primes B cells to recruit, engage and respond to T cell help (signal 2). Failure to receive signal 2 within a defined time window results in B cell apoptosis, yet the mechanisms that enforce dependence on co-stimulation are incompletely understood. Nr4a1-3 encode a small family of orphan nuclear receptors that are rapidly induced by B cell antigen receptor stimulation. Here, we show that Nr4a1 and Nr4a3 play partially redundant roles to restrain B cell responses to antigen in the absence of co-stimulation and do so, in part, by repressing the expression of BATF and, consequently, MYC. The NR4A family also restrains B cell access to T cell help by repressing expression of the T cell chemokines CCL3 and CCL4, as well as CD86 an","dates":{"release":"2020-01-01T00:00:00Z","publication":"2020 Oct","modification":"2026-04-30T03:08:59.466Z","creation":"2022-02-10T08:17:36.494Z"},"accession":"S-EPMC8081071","cross_references":{"pubmed":["32868928"],"doi":["10.1038/s41590-020-0765-7"]}}