ArticleEMBO reports2022
Single cell clonal analysis identifies an AID-dependent pathway of plasma cell differentiation.
Article in EMBO reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- AID and TET2 cooperate to demethylate Irf4 for plasma cell fate in germinal center B cells.The Journal of experimental medicine · 2026Article
- Integrated single cell multiomic profiling and functional validation reveal distinct cellular routes to human plasma cell differentiation.bioRxiv : the preprint server for biology · 2026Article
- RIF1 integrates DNA repair and transcriptional requirements during the establishment of humoral immune responses.Nature communications · 2025Article
- Defective mitochondria remodelling in B cells leads to an aged immune response.Nature communications · 2024Article
- Single cell clonal analysis identifies an AID-dependent pathway of plasma cell differentiation.EMBO reports · 2022Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Germinal centers (GC) are microstructures where B cells that have been activated by antigen can improve the affinity of their B cell receptors and differentiate into memory B cells (MBCs) or antibody-secreting plasma cells. Here, we have addressed the role of activation-induced deaminase (AID), which initiates somatic hypermutation and class switch recombination, in the terminal differentiation of GC B cells. By combining single cell transcriptome and immunoglobulin clonal analysis in a mouse model that traces AID-experienced cells, we have identified a novel subset of late-prePB cells (L-prePB), which shares the strongest clonal relationships with plasmablasts (PBs). Mice lacking AID have various alterations in the size and expression profiles of transcriptional clusters. We find that AID deficiency leads to a reduced proportion of L-prePB cells and severely impairs transitions between the L-prePB and the PB subsets. Thus, AID shapes the differentiation fate of GC B cells by enabling PB generation from a prePB state.
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Registered trials
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