Evidence map›Paper›PMID 38969872›Full record

ArticleNature immunology2024

Epigenetic recording of stimulation history reveals BLIMP1-BACH2 balance in determining memory B cell fate upon recall challenge.

Wen Shao, Yifeng Wang, Qian Fang, Wenjuan Shi, Hai Qi

Abstract read
PubMed Publisher
In one paragraph

Article in Nature immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

30 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Epstein-Barr virus (EBV) infection causes human germinal center B cell-derived lymphomas in the absence of EBNA2 expression.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  7. Clonal dynamics of germinal center refueling by secondary immunization.bioRxiv : the preprint server for biology · 2026
    Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. The multilayered identity of B cell memory.Cellular & molecular immunology · 2026
    Review
  15. Article
  16. Review
  17. Article
  18. Review
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Wen Shao *Tsinghua-Peking Center for Life Sciences, Beijing, China.
Yifeng Wang *Tsinghua-Peking Center for Life Sciences, Beijing, China.
Qian FangTsinghua-Peking Center for Life Sciences, Beijing, China.
Wenjuan ShiSXMU-Tsinghua Collaborative Innovation Center for Frontier Medicine, Shanxi Medical University, Taiyuan, China.
Hai QiTsinghua-Peking Center for Life Sciences, Beijing, China. qihai@tsinghua.edu.cn.ORCID http://orcid.org/0000-0001-5475-3989

Funding

China Postdoctoral Science Foundation 2022T150351Ministry of Science and Technology of the People's Republic of China (Chinese Ministry of Science and Technology) 2018YFE0200300National Natural Science Foundation of China (National Science Foundation of China) 31900629National Natural Science Foundation of China (National Science Foundation of China) 32200725National Natural Science Foundation of China (National Science Foundation of China) 81621002
6 · The paper itself

Abstract

Memory B cells (MBCs) differentiate into plasma cells (PCs) or germinal centers (GCs) upon antigen recall. How this decision is programmed is not understood. We found that the relative strength between two antagonistic transcription factors, B lymphocyte-induced maturation protein 1 (BLIMP1) and BTB domain and CNC homolog 2 (BACH2), progressively increases in favor of BLIMP1 in antigen-responding B cells through the course of primary responses. MBC subsets that preferentially produce secondary GCs expressed comparatively higher BACH2 but lower BLIMP1 than those predisposed for PC development. Skewing the BLIMP1-BACH2 balance in otherwise fate-predisposed MBC subsets could switch their fate preferences. Underlying the changing BLIMP1-over-BACH2 balance, we observed progressively increased accessibilities at chromatin loci that are specifically opened in PCs, particularly those that contain interferon-sensitive response elements (ISREs) and are controlled by interferon regulatory factor 4 (IRF4). IRF4 is upregulated by B cell receptor, CD40 or innate receptor signaling and it induces graded levels of PC-specifying epigenetic imprints according to the strength of stimulation. By analyzing history-stamped GC B cells, we found progressively increased chromatin accessibilities at PC-specific, IRF4-controlled gene loci over time. Therefore, the cumulative stimulation history of B cells is epigenetically recorded in an IRF4-dependent manner, determines the relative strength between BLIMP1 and BACH2 in individual MBCs and dictates their probabilities to develop into GCs or PCs upon restimulation.

Indexed as

Basic-Leucine Zipper Transcription FactorsCell DifferentiationEpigenesis, GeneticGerminal CenterImmunologic MemoryInterferon Regulatory FactorsMemory B CellsPlasma CellsPositive Regulatory Domain I-Binding Factor 1AnimalsInterferon Regulatory Factor-4Lymphocyte ActivationMiceMice, Inbred C57BLSignal TransductionBach2 protein, mouseBasic-Leucine Zipper Transcription FactorsInterferon Regulatory Factor-4Interferon Regulatory FactorsPositive Regulatory Domain I-Binding Factor 1Prdm1 protein, mouse

Identifiers

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.