Transcription Factors IRF8 and PU.1 Are Required for Follicular B Cell Development and BCL6‐driven Germinal Center Responses
Open accessAbstract
The IRF and Ets families of transcription factors regulate the expression of a range of genes involved in immune cell development and function. However, the understanding of the molecular mechanisms of each family member has been limited due to their redundancy and broad effects on multiple lineages of cells. Here, we report that double deletion of floxed Irf8 and Spi1 (encoding PU.1) by Mb1-Cre (designated DKO mice) in the B cell lineage resulted in severe defects in the development of follicular and germinal center (GC) B cells. Class-switch recombination and antibody affinity maturation were also compromised in DKO mice. RNA-seq (sequencing) and ChIP-seq analyses revealed distinct IRF8 and PU.1 target genes in follicular and activated B cells. DKO B cells had diminished expression of target genes vital for maintaining follicular B cell identity and GC development. Moreover, our findings reveal that expression of B-cell lymphoma protein 6 (BCL6), which is critical for development of germinal center B cells, is dependent on IRF8 and PU.1 in vivo, providing a mechanism for the critical role for IRF8 and PU.1 in the development of GC B cells.
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PU.1 functions as a pioneer transcriptional factor that establishes enhancer accessibility in myeloid lineage cells and directly induces expression of other transcriptional factors, such as IRF8 and MEF2C.
“Especially, PU.1 functions as a pioneer transcriptional factor that establishes enhancer accessibility in myeloid lineage cells and directly induces expression of other transcriptional factors (e.g., IRF8, MEF2C) [29, 64, 69, 70].”
From Targeting Microglial Transcriptional Reprogramming as a Therapy Strategy for Alzheimer's Disease (2026) · cites this paper as [69]
In “Disrupted Germinal Center Responses in DKO Mice” (page unavailable), the paper identifies Mef2c as a direct target of IRF8 and PU.1 in follicular B cells. It does not establish that PU.1 acts as a pioneer factor to open enhancers in myeloid cells or that it directly induces IRF8 expression. (LLM, conf=0.84)
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B Cells and Microbiota in Autoimmunity
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Molecular Subgroups of Diffuse Large B Cell Lymphoma: Biology and Implications for Clinical Practice
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The role of CD180 in hematological malignancies and inflammatory disorders
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IRF8 is a transcriptional activator of CD37 expression in diffuse large B-cell lymphoma
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ANP32B suppresses B‐cell acute lymphoblastic leukemia through activation of PU .1 in mice
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IRF8 regulates efficacy of therapeutic anti‐CD20 monoclonal antibodies
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Comprehensive Analysis Identified ETV7 as a Potential Prognostic Biomarker in Bladder Cancer
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Recent advances in host-focused molecular tools for investigating host-gut microbiome interactions
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Loss of synergistic transcriptional feedback loops drives diverse B-cell cancers
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Epitope-focused vaccine immunogens design using tailored horseshoe-shaped scaffold
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CRISPR/Cas9 editing reveals IRF8 regulated gene signatures restraining plasmablast differentiation
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Generation and characterization of the Eµ-Irf8 mouse model
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Axes of biological variation in diffuse large B cell lymphoma
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Langerhans cells drive Tfh and B cell responses independent of canonical cytokine signals
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The circulating IL‐35+ regulatory B cells are associated with thyroid associated opthalmopathy
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IRF8 as durable architect of the microglial chromatin landscape
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Decreased PU.1 expression in mature B cells induces lymphomagenesis
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Nanoparticle Immunoadjuvant Complexes Augment Germinal Center Responses to Vaccination
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Targeting Microglial Transcriptional Reprogramming as a Therapy Strategy for Alzheimer's Disease
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- Authors
- Wang, H., Jain, S., Li, P., Lin, J.-X., Oh, J., Qi, C., Gao, Y., Sun, J., Sakai, T., Naghashfar, Z., Abbasi, S., Kovalchuk, A. L., Bolland, S., Nutt, S. L., Leonard, W. J., & Morse, H. C.
- Affiliations
- National Institutes of Health (US)
- Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852;
- The University of Melbourne (AU)
- ORCID
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2019-04-18
- Volume
- 116
- Issue
- 19
- Pages
- 9511-9520
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC6511064
- OpenAlex
- W2937775576
- Cited by
- 81
- References
- 76
- Citations by year
- 2026: 14 · 2025: 10 · 2024: 11 · 2023: 11 · 2022: 9 · 2021: 10 · 2020: 11 · 2019: 5
- FWCI
- 3.50
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- Medical Research Council
- National Health and Medical Research Council (1054925, 1058238, 1054925, 1058238)
- National Heart, Lung, and Blood Institute
- National Institute of Allergy and Infectious Diseases
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Lymphoma Diagnosis and Treatment
- Keywords
- IRF8, PU.1, follicular B cells, germinal center, BCL6, class switch recombination, affinity maturation, transcription factor target genes, B cell development
- MeSH terms
- Interferon Regulatory Factor-8, Proto-Oncogene Protein Spi-1, Animals, B-Lymphocytes, Lymphocyte Activation, Proto-Oncogene Proteins, Trans-Activators, Immunoglobulin Class Switching, Mice, Knockout, Germinal Center, Interferon Regulatory Factors, Mice, Proto-Oncogene Proteins c-bcl-6
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