ArticleNature communications2022
A p38α-BLIMP1 signalling pathway is essential for plasma cell differentiation.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.
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- Mechanistic study of compound Muniziqi granule on lupus nephritis in MRL/lpr mice: insights from transcriptomics and experimental validation.Lupus science & medicine · 2026Article
- Derlin-3 manipulates the endoplasmic reticulum stress and IgG4 secretion of plasma cells in lung adenocarcinoma.Oncogene · 2025Article
- Berberine as a natural immunomodulator of B lymphocytes.Inflammopharmacology · 2025Review
- Interferon regulatory factor 4 mediates nonenzymatic IRE1 dependency in multiple myeloma cells.PLoS biology · 2025Article
- GSTP1 improves CAR-T cell proliferation and cytotoxicity to combat lymphoma.Frontiers in immunology · 2025Article
- Systems Biology Methods via Genome-Wide RNA Sequences to Investigate Pathogenic Mechanisms for Identifying Biomarkers and Constructing a DNN-Based Drug-Target Interaction Model to Predict Potential Molecular Drugs for Treating Atopic Dermatitis.International journal of molecular sciences · 2024Article
- Short-Chain Fatty Acids Alleviate Vancomycin-Caused Humoral Immunity Attenuation in Rabies-Vaccinated Mice by Promoting the Generation of Plasma Cells via Akt-mTOR Pathway.Journal of virology · 2023Article
- High-throughput CRISPR technology: a novel horizon for solid organ transplantation.Frontiers in immunology · 2023Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Plasma cells (PC) are antibody-secreting cells and terminal effectors in humoral responses. PCs differentiate directly from activated B cells in response to T cell-independent (TI) antigens or from germinal center B (GCB) cells in T cell-dependent (TD) antigen-induced humoral responses, both of which pathways are essentially regulated by the transcription factor BLIMP1. The p38 mitogen-activated protein kinase isoforms have already been implicated in B cell development, but the precise role of p38α in B cell differentiation is still largely unknown. Here we show that PC differentiation and antibody responses are severely impaired in mice with B cell-specific deletion of p38α, while B cell development and the GCB cell response are spared. By utilizing a Blimp1 reporter mouse model, we show that p38α-deficiency results in decreased BLIMP1 expression. p38α-driven BLIMP1 up-regulation is required for both TI and TD PCs differentiation. By combining CRISPR/Cas9 screening and other approaches, we identify TCF3, TCF4 and IRF4 as downstream effectors of p38α to control PC differentiation via Blimp1 transcription. This study thus identifies an important signalling pathway underpinning PC differentiation upstream of BLIMP1, and points to a highly specialized and non-redundant role for p38α among p38 isoforms.
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