ArticleNature communications2017
IL-2 imprints human naive B cell fate towards plasma cell through ERK/ELK1-mediated BACH2 repression.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 1 of them a synthesis that pooled it.
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Who cites it
72 citing papers in PubMed, 1 synthesis or guideline pooled it, 105 citations in OpenAlex.
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- Integrated single cell multiomic profiling and functional validation reveal distinct cellular routes to human plasma cell differentiation.bioRxiv : the preprint server for biology · 2026Article
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- IL-2Rα is dispensable for murine B cell development and humoral response.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- ROCK1 promotes B cell differentiation and proteostasis under stress through the heme-regulated proteins, BACH2 and HRI.JCI insight · 2025Article
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- MAPK/ERK signaling pathway in rheumatoid arthritis: mechanisms and therapeutic potential.PeerJ · 2025Review
- Subclinical ketosis in postpartum dairy cows alters the adipose tissue immunological profile in a depot-specific manner.Frontiers in immunology · 2025Article
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- EfficientImmune network · 2024Article
12 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Plasma cell differentiation is a tightly regulated process that requires appropriate T cell helps to reach the induction threshold. To further understand mechanisms by which T cell inputs regulate B cell fate decision, we investigate the minimal IL-2 stimulation for triggering human plasma cell differentiation in vitro. Here we show that the timed repression of BACH2 through IL-2-mediated ERK/ELK1 signalling pathway directs plasma cell lineage commitment. Enforced BACH2 repression in activated B cells unlocks the plasma cell transcriptional program and induces their differentiation into immunoglobulin M-secreting cells. RNA-seq and ChIP-seq results further identify BACH2 target genes involved in this process. An active regulatory region within the BACH2 super-enhancer, under ELK1 control and differentially regulated upon B-cell activation and cellular divisions, helps integrate IL-2 signal. Our study thus provides insights into the temporal regulation of BACH2 and its targets for controlling the differentiation of human naive B cells.
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