{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Song W"],"funding":["NCATS NIH HHS","NIAMS NIH HHS"],"pagination":["290-307.e5"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8965751"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["55(2)"],"pubmed_abstract":["Tbet<sup>+</sup>CD11c<sup>+</sup> B cells arise during type 1 pathogen challenge, aging, and autoimmunity in mice and humans. Here, we examined the developmental requirements of this B cell subset. In acute infection, T follicular helper (Tfh) cells, but not Th1 cells, drove Tbet<sup>+</sup>CD11c<sup>+</sup> B cell generation through proximal delivery of help. Tbet<sup>+</sup>CD11c<sup>+</sup> B cells developed prior to germinal center (GC) formation, exhibiting phenotypic and transcriptional profiles distinct from GC B cells. Fate tracking revealed that most Tbet<sup>+</sup>CD11c<sup>+</sup> B cells developed independently of GC entry and cell-intrinsic Bcl6 expression. Tbet<sup>+</sup>CD11c<sup>+</sup> and GC B cells exhibited minimal repertoire overlap, indicating distinct developmental pathways. As the infection resolved, Tbet<sup>+</sup>CD11c<sup>+</sup> B cells localized to the marginal zone where splenic retention depended on integrins LFA-1 and VLA-4, forming a competitive memory subset that contributed to antibody production and secondary GC seeding upon rechallenge. Therefore, Tbet<sup>+</sup>CD11c<sup>+</sup> B cells comprise a GC-independent memory subset capable of rapid and robust recall responses."],"journal":["Immunity"],"pubmed_title":["Development of Tbet- and CD11c-expressing B cells in a viral infection requires T follicular helper cells outside of germinal centers."],"pmcid":["PMC8965751"],"funding_grant_id":["R01 AR040072","R01 AR073912","K01 AR067892","R37 AR040072","UL1 TR001863","R01 AR074545"],"pubmed_authors":["Rubtsova K","Lemenze A","Laidlaw BJ","Sanchez GM","Chernova I","Antao OQ","Condiff E","Steach H","Craft J","Angeletti D","Song W","Zembrzuski K","Weinstein JS"],"additional_accession":[]},"is_claimable":false,"name":"Development of Tbet- and CD11c-expressing B cells in a viral infection requires T follicular helper cells outside of germinal centers.","description":"Tbet<sup>+</sup>CD11c<sup>+</sup> B cells arise during type 1 pathogen challenge, aging, and autoimmunity in mice and humans. Here, we examined the developmental requirements of this B cell subset. In acute infection, T follicular helper (Tfh) cells, but not Th1 cells, drove Tbet<sup>+</sup>CD11c<sup>+</sup> B cell generation through proximal delivery of help. Tbet<sup>+</sup>CD11c<sup>+</sup> B cells developed prior to germinal center (GC) formation, exhibiting phenotypic and transcriptional profiles distinct from GC B cells. Fate tracking revealed that most Tbet<sup>+</sup>CD11c<sup>+</sup> B cells developed independently of GC entry and cell-intrinsic Bcl6 expression. Tbet<sup>+</sup>CD11c<sup>+</sup> and GC B cells exhibited minimal repertoire overlap, indicating distinct developmental pathways. As the infection resolved, Tbet<sup>+</sup>CD11c<sup>+</sup> B cells localized to the marginal zone where splenic retention depended on integrins LFA-1 and VLA-4, forming a competitive memory subset that contributed to antibody production and secondary GC seeding upon rechallenge. Therefore, Tbet<sup>+</sup>CD11c<sup>+</sup> B cells comprise a GC-independent memory subset capable of rapid and robust recall responses.","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Feb","modification":"2026-05-31T13:02:06.904Z","creation":"2025-04-06T21:48:54.434Z"},"accession":"S-EPMC8965751","cross_references":{"pubmed":["35090581"],"doi":["10.1016/j.immuni.2022.01.002"]}}