ArticleProceedings of the National Academy of Sciences of the United States of America2013
The transcription factor Interferon Regulatory Factor 4 is required for the generation of protective effector CD8+ T cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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Who cites it
62 citing papers in PubMed, 96 citations in OpenAlex.
- Interferon regulatory factors orchestrate CD8International journal of molecular medicine · 2026Review
- IL-21 Selectively Augments Cytotoxic Potential of Antigen-Activated MAIT Cells.European journal of immunology · 2026Article
- Integration of single-cell and bulk RNA sequencing reveals divergent T-cell immune circuits and a shared osteo-immune pathway in spinal tuberculosis and brucellar spondylitis.Frontiers in cellular and infection microbiology · 2026Article
- Interferon regulatory factor 4 as a context-dependent regulator of inflammation: transcriptional and epigenetic control, skin diseases, and translational challenges.Frontiers in immunology · 2026Review
- Disrupted priming within draining lymph nodes drives immune quiescence in gastric cancer.bioRxiv : the preprint server for biology · 2025Article
- Development of potent HLA-A02:01-restricted peptide-based cytotoxic T-cells against SARS-CoV-2 infections in patients awaiting a kidney transplant.Frontiers in immunology · 2025Article
- Interferon Regulatory Factor 4 dose-dependently controls peripheral Treg cell differentiation and homeostasis by modulating chromatin accessibility in mice.Frontiers in immunology · 2025Article
- The multiple roles of interferon regulatory factor family in health and disease.Signal transduction and targeted therapy · 2024Review
- IL-2 delivery to CD8Nature communications · 2024Article
- Interferon regulatory factor 4 plays a pivotal role in the development of aGVHD-associated colitis.Oncoimmunology · 2024Article
- Pyrimidine de novo synthesis inhibition selectively blocks effector but not memory T cell development.Nature immunology · 2023Article
- A multimorphic mutation in IRF4 causes human autosomal dominant combined immunodeficiency.Science immunology · 2023Article
- IRF4 is required for migration of CD4Frontiers in immunology · 2023Article
- Regulatory effects of IRF4 on immune cells in the tumor microenvironment.Frontiers in immunology · 2023Review
- Translation factor eIF5a is essential for IFNγ production and cell cycle regulation in primary CD8Nature communications · 2022Article
- Expression of NAC1 Restrains the Memory Formation of CD8Viruses · 2022Article
- Dapl1 controls NFATc2 activation to regulate CD8Nature cell biology · 2022Article
- Article
- Ablation of BATF Alleviates Transplant RejectionFrontiers in immunology · 2022Article
- Interferon regulatory factor 4 controls effector functions of CD8Proceedings of the National Academy of Sciences of the United States of America · 2021Article
2 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Robust cytotoxic CD8(+) T-cell response is important for immunity to intracellular pathogens. Here, we show that the transcription factor IFN Regulatory Factor 4 (IRF4) is crucial for the protective CD8(+) T-cell response to the intracellular bacterium Listeria monocytogenes. IRF4-deficient (Irf4(-/-)) mice could not clear L. monocytogenes infection and generated decreased numbers of L. monocytogenes-specific CD8(+) T cells with impaired effector phenotype and function. Transfer of wild-type CD8(+) T cells into Irf4(-/-) mice improved bacterial clearance, suggesting an intrinsic defect of CD8(+) T cells in Irf4(-/-) mice. Following transfer into wild-type recipients, Irf4(-/-) CD8(+) T cells became activated and showed initial proliferation upon L. monocytogenes infection. However, these cells could not sustain proliferation, produced reduced amounts of IFN-γ and TNF-α, and failed to acquire cytotoxic function. Forced IRF4 expression in Irf4(-/-) CD8(+) T cells rescued the defect. During acute infection, Irf4(-/-) CD8(+) T cells demonstrated diminished expression of B lymphocyte-induced maturation protein-1 (Blimp-1), inhibitor of DNA binding (Id)2, and T-box expressed in T cells (T-bet), transcription factors programming effector-cell generation. IRF4 was essential for expression of Blimp-1, suggesting that altered regulation of Blimp-1 contributes to the defects of Irf4(-/-) CD8(+) T cells. Despite increased levels of B-cell lymphoma 6 (BCL-6), Eomesodermin, and Id3, Irf4(-/-) CD8(+) T cells showed impaired memory-cell formation, indicating additional functions for IRF4 in this process. As IRF4 governs B-cell and CD4(+) T-cell differentiation, the identification of its decisive role in peripheral CD8(+) T-cell differentiation, suggests a common regulatory function for IRF4 in adaptive lymphocytes fate decision.
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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 OpenQuestion graph.