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Showing IRF8 — ICSBP is a alias.

IRF8

Interferon regulatory factor 8 · UniProt Q02556

Length
426 aa
Mass
48.4 kDa
Annotated
2026-06-10
100 papers in source corpus 54 papers cited in narrative 53 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 9/9 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

IRF8 (ICSBP) is an IFN-γ-inducible transcription factor that serves as a master regulator of myeloid and dendritic cell fate, hematopoietic homeostasis, and innate immunity (PMID:8861914, PMID:8321202). Its induction is driven by STAT1 acting through a palindromic IFN response element in the Irf8 promoter (PMID:8321202), and it operates through three functional modules: a DNA-binding domain, a transcriptional repressor domain, and an IRF-association domain (IAD) that mediates combinatorial partnerships with other transcription factors (PMID:7768900). Through these partnerships—with PU.1, IRF-1, IRF-2, IRF-3, IRF-4, BATF, NFAT, and the Ets factor TEL—IRF8 binds ISRE, EICE, and composite Ets/IRF elements to either activate or repress targets depending on partner context, including TEL/HDAC3-mediated repressive feedback at the ISRE (PMID:7768900, PMID:12370291, PMID:12876285, PMID:17200120, PMID:21228327, PMID:29233972). At the lineage level IRF8 drives differentiation of monocytes, macrophages, and dendritic cells while extinguishing neutrophil/granulocyte production, with dose-dependent enhancer usage (a RUNX-CBFβ-driven +56-kb enhancer for the broad myeloid program, transient +41-kb and +32-kb enhancers for cDC1 specification versus maturation) determining cDC1, monocyte, or neutrophil fate, and continuous IRF8 activity required to maintain committed cDC1 identity (PMID:10981959, PMID:22238324, PMID:31406378, PMID:31406377, PMID:35830859, PMID:33603226). IRF8 functions as a myeloid tumor suppressor that antagonizes BCR-ABL-driven myeloproliferation by activating cell-cycle and pro-apoptotic programs (p15Ink4b, Blimp-1, acid ceramidase) and repressing growth-promoting targets (c-Myc, bcl-2, β-catenin via Gas2), and its loss accelerates progression to blast crisis and AML (PMID:10648600, PMID:12933588, PMID:14656881, PMID:14976051, PMID:20679491, PMID:21487040, PMID:26683374). In innate immunity IRF8 transcribes Naip genes to license NLRC4 inflammasome activation, drives autophagy gene expression for bacterial clearance, and cooperates with IRF3 for IFN-β induction (PMID:25775030, PMID:29576451, PMID:33535228, PMID:21228327). Beyond transcription, IRF8 acts non-transcriptionally in the cGAS-STING pathway: phosphorylation at Ser151 releases its IAD to bind STING, promoting STING polymerization and TBK1-mediated signaling (PMID:35973990). IRF8 also establishes and maintains microglial identity through stepwise enhancer activation, chromatin accessibility, and DNA methylation alongside Sall1 and PU.1 (PMID:39313544, PMID:30484118). Human IRF8 deficiency produces a graded loss of dendritic cell subsets (PMID:32735845).

Mechanistic history

Synthesis pass · year-by-year structured walk · 18 steps
  1. 1993 High

    Establishing how IRF8 is itself controlled, the discovery that its promoter carries a STAT1-bound IFN response element defined IRF8 as a downstream effector of IFN-γ signaling.

    Evidence Gel shift, reporter assays, and antibody supershift on the murine ICSBP promoter

    PMID:8321202

    Open questions at the time
    • Did not address IRF8's own transcriptional targets
    • Other inducing signals beyond IFN-γ/STAT1 not mapped
  2. 1995 High

    Dissecting the protein into a DNA-binding domain, a repressor domain, and an IRF-association domain explained how IRF8 could act through partner-dependent combinatorial assemblies.

    Evidence Domain deletion mutagenesis, GAL4/VP16 fusions, EMSA, and co-IP with IRF-1 and IRF-2

    PMID:7768900

    Open questions at the time
    • Did not establish in vivo physiological partners
    • Structural basis of IAD interaction not resolved
  3. 1996 High

    The null mouse demonstrated that IRF8 is essential for hematopoietic homeostasis, linking its loss to a CML-like myeloproliferative syndrome and immunodeficiency.

    Evidence ICSBP-/- knockout mice with bone marrow transfer and phenotypic analysis

    PMID:8861914

    Open questions at the time
    • Did not identify the direct target genes underlying myeloproliferation
    • Cell-intrinsic versus environmental contributions not separated
  4. 2000 High

    Gain-of-function and target studies showed IRF8 actively drives macrophage differentiation while repressing granulocyte genes and is the principal activator of IL-12 p40, defining its myeloid lineage-instructive role.

    Evidence Retroviral rescue of ICSBP-/- progenitors, differentiation assays, and IL-12 p40 promoter reporter/binding assays

    PMID:10861061 PMID:10981959

    Open questions at the time
    • Full set of macrophage versus granulocyte target genes incomplete
    • Mechanism of partner selection at distinct promoters unresolved
  5. 2000 High

    Demonstrating IRF8 downregulation by BCR-ABL and its suppression of CML in vivo established IRF8 as a bona fide myeloid tumor suppressor.

    Evidence Retroviral co-expression with BCR-ABL, colony formation, and murine bone marrow transplantation

    PMID:10648600

    Open questions at the time
    • Direct transcriptional targets mediating tumor suppression not yet defined at this stage
  6. 2003 Medium

    Mechanistic dissection revealed IRF8's tumor-suppressive output operates through repression of c-Myc (via Blimp-1/METS), bcl-2, and PTPN13/Fap-1, and activation of p15Ink4b, linking IRF8 to growth arrest and apoptosis sensitivity.

    Evidence Conditional ICSBP/ER systems, reporter assays, EMSA, and apoptosis assays in BCR/ABL-transformed cells

    PMID:12933588 PMID:14656881 PMID:14976051 PMID:18195016

    Open questions at the time
    • Direct versus indirect target relationships partly inferred
    • Single-lab findings for several targets
  7. 2002 High

    Identifying partner-dependent activity—NFAT and TEL/HDAC3 associations, plus the requirement for DNA binding and IRF interaction—explained how IRF8 toggles between activation and repression at the same elements.

    Evidence Mass spectrometry of ISRE-bound proteins, co-IP, ChIP, reporter assays, and mutant rescue in DC differentiation

    PMID:12370291 PMID:12393459 PMID:12417340 PMID:12876285

    Open questions at the time
    • Determinants of repressive versus activating partner recruitment not fully defined
    • Some interactions characterized in single labs
  8. 2002 High

    Knockout and chimera studies established IRF8's selective requirement for CD8α+ DC and plasmacytoid DC development, anchoring its role in DC subset specification.

    Evidence ICSBP-/- mouse and bone marrow chimera analysis with flow cytometry and RT-PCR

    PMID:12393690 PMID:12461077

    Open questions at the time
    • Enhancer-level control of subset specification not yet known
    • Did not resolve dose-dependence of fate decisions
  9. 2005 High

    The BXH2 R294C IAD mutation linked a specific lesion to loss of partner interaction, IL-12 defects, and myeloproliferation, proving the IAD is functionally essential in vivo.

    Evidence Positional cloning, sequencing, transactivation reporter assays, and DC subset phenotyping in BXH2 mice

    PMID:15781580 PMID:18055870

    Open questions at the time
    • Why pDC development is spared while CD8α+ DC is lost not fully explained mechanistically
  10. 2008 High

    Direct binding studies in B-cell and myeloid contexts showed IRF8 regulates lineage transcription factors (Sfpi1/PU.1, Ebf1) and forms composite complexes with PU.1 and IRF-2, formalizing its combinatorial logic in lineage specification.

    Evidence ChIP, reporter assays, and mutant rescue in IRF8-/- HSCs; EMSA with phosphorylation mutants

    PMID:17200120 PMID:18799728 PMID:28008797

    Open questions at the time
    • Post-translational control of partner recruitment (Tyr/Ser phosphorylation, deacetylation) only partly mapped
  11. 2013 Medium

    Multiple studies positioned IRF8 within signaling circuits controlling its abundance—STAT3/STAT5 and tumor-derived G-CSF suppress it to drive MDSC/cDC defects, while Wnt/β-catenin activates it—linking IRF8 levels to immune and oncogenic outcomes.

    Evidence Genetic models, cytokine pathway analysis, tumor models, and β-catenin epistasis

    PMID:24091328 PMID:24101380 PMID:29233972 PMID:29593283

    Open questions at the time
    • Quantitative thresholds of IRF8 needed for each outcome not defined here
    • Several single-lab mechanisms
  12. 2015 High

    IRF8 was shown to directly transcribe autophagy genes and (with PU.1) Naip/NLRP3 inflammasome components, extending its role from lineage control to effector innate immune functions.

    Evidence ChIP, autophagic flux and bacterial clearance assays, infection assays, and caspase activation in Irf8-/- macrophages

    PMID:25775030 PMID:29576451 PMID:32205422 PMID:33535228 PMID:33897697

    Open questions at the time
    • Selectivity for NLRC4 versus other inflammasomes mechanistically partial
    • Brd4 contribution to Naip control single-lab
  13. 2018 High

    Cell-intrinsic studies defined an IL-12/STAT4/IRF8/Zbtb32 axis driving NK cell proliferation and antiviral protection through epigenetic remodeling of the Irf8 locus, broadening IRF8 beyond myeloid lineages.

    Evidence Cell-intrinsic KO, STAT4 requirement, epigenetic profiling, and MCMV infection

    PMID:29858012

    Open questions at the time
    • Direct NK-specific IRF8 target genome not fully cataloged
  14. 2019 High

    CRISPR enhancer deletion and single-cell genomics established a dose- and enhancer-dependent code (+56-kb, +41-kb, +32-kb; Nfil3-Zeb2-Id2 circuit) that times Irf8 expression to specify versus maintain cDC1 identity.

    Evidence CRISPR enhancer deletion, ATAC-seq, scRNA-seq, genetic epistasis, and conditional deletion in committed cDC1

    PMID:31406377 PMID:31406378 PMID:33603226 PMID:35830859 PMID:41

    Open questions at the time
    • Trans-factors reading each enhancer not all identified
    • How IRF8 dose is sensed at target promoters unresolved
  15. 2021 High

    Identifying ZMYND8-BRD4 activation of IRF8 enhancers and an IRF8-MEF2D circuit revealed how IRF8 is co-opted as an AML dependency, connecting enhancer regulation to leukemic survival.

    Evidence ChIP-seq, protein interaction mapping, and in vitro/in vivo ZMYND8 knockout

    PMID:34358447

    Open questions at the time
    • Therapeutic tractability of the circuit not addressed in this synthesis
  16. 2022 High

    The discovery that Ser151-phosphorylated IRF8 binds STING to promote its polymerization revealed a transcription-independent role in cGAS-STING/TBK1 innate immune signaling.

    Evidence Phospho-mutant analysis, co-IP, STING polymerization assays, and HSV-1 infection of IRF8-deficient monocytes

    PMID:35973990

    Open questions at the time
    • Kinase responsible for Ser151 phosphorylation not identified here
    • Interplay between transcriptional and non-transcriptional roles unresolved
  17. 2024 High

    Multi-omic epigenomic profiling showed IRF8 stepwise establishes microglial enhancer accessibility and DNA methylation with Sall1 and PU.1, and is continuously required to maintain microglial identity versus disease-associated states.

    Evidence ChIP-seq, ATAC-seq, scRNA/scATAC-seq, bisulfite sequencing, and conditional deletion in the 5xFAD model

    PMID:30484118 PMID:39313544

    Open questions at the time
    • Mechanism coupling IRF8 binding to DNA methylation changes not defined
    • Relevance to human microglial disease not directly tested
  18. 2022 High

    Cell-type-specific deletion and post-transcriptional regulation studies placed IRF8 at the interface of tumor immunity—TAM IRF8 drives CTL exhaustion, while FTO/m6A and miR-22 tune IRF8 levels to control differentiation and malignancy.

    Evidence TAM-specific and tumor conditional KO, antigen presentation/exhaustion assays, m6A-seq, RIP-seq, and luciferase 3'UTR reporters

    PMID:23251709 PMID:32735845 PMID:36288724 PMID:36478193

    Open questions at the time
    • Context-dependent pro- versus anti-tumor roles of IRF8 not fully reconciled
    • Some post-transcriptional mechanisms single-lab

Open questions

Synthesis pass · forward-looking unresolved questions
  • How IRF8's transcriptional and non-transcriptional (STING) activities are coordinated within a single cell, and what upstream kinases and dose-sensing mechanisms integrate the diverse signaling inputs into context-specific enhancer choice, remains unresolved.
  • No unified model linking Ser151/Tyr phosphorylation events to transcriptional output
  • Kinase(s) and full PTM code not defined
  • Determinants of activator-versus-repressor partner selection incompletely mapped

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 8 GO:0003677 DNA binding 5 GO:0098772 molecular function regulator activity 1
Localization
GO:0005634 nucleus 3 GO:0005829 cytosol 1
Pathway
R-HSA-1266738 Developmental Biology 5 R-HSA-168256 Immune System 5 R-HSA-1643685 Disease 4 R-HSA-74160 Gene expression (Transcription) 4 R-HSA-4839726 Chromatin organization 3 R-HSA-162582 Signal Transduction 2 R-HSA-9612973 Autophagy 1
Partners
BATFIRF1IRF2IRF3IRF4NFATC1PU.1STING1

Evidence

Reading pass · 53 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1996 Targeted null mutation of ICSBP (IRF8) in mice causes immunodeficiency with impaired IFN-γ production and a CML-like myeloproliferative syndrome progressing to fatal blast crisis, establishing IRF8 as a regulator of hematopoietic progenitor cell proliferation and differentiation. Gene knockout mouse model (ICSBP-/- mice), bone marrow transfer, phenotypic analysis Cell High 8861914
1993 The murine ICSBP gene contains a palindromic IFN response element (pIRE, TTCNNGGAA) in its promoter that confers IFN-γ induction via binding of the 91-kDa ISGF3α subunit (STAT1), establishing ICSBP as an IFN-γ-inducible gene regulated by STAT1. Gel mobility shift assay, heterologous promoter reporter assay, antibody supershift Molecular and cellular biology High 8321202
1995 ICSBP contains at least three independent functional domains: a DNA-binding domain (DBD, aa 1-121), a transcriptional repressor domain, and an IRF-association domain (IAD) that mediates protein-protein interaction with IRF-1 and IRF-2 in vitro and in vivo. Domain deletion mutagenesis, VP16/GAL4 fusion constructs, electrophoretic mobility shift assay (EMSA), co-IP The Journal of biological chemistry High 7768900
1994 ICSBP acts as a conditional repressor of IFN-stimulated response element (ISRE)-containing promoters in hematopoietic cells; IRF-1 competes with ICSBP for ISRE binding and alleviates ICSBP-mediated repression, revealing a balance between positive (IRF-1) and negative (ICSBP) regulators of ISG expression. Reporter gene assay, EMSA competition assay International immunology Medium 7526889
2000 ICSBP drives myeloid progenitor differentiation toward mature macrophages and represses granulocyte-specific genes; retroviral transduction of ICSBP into ICSBP-/- myeloid progenitors induced growth arrest, macrophage-specific gene expression, phagocytic activity, and inhibited G-CSF-mediated granulocytic differentiation. Retroviral transduction, in vitro differentiation assay, target DNA binding assay Immunity High 10981959
2000 ICSBP (IRF8) is required for IL-12 p40 transcription in macrophages; it acts as a principal transcriptional activator of the IL-12 p40 promoter through the Ets binding site via protein-protein interaction, and synergizes with IRF-1. ICSBP-/- macrophage-like cells fail to induce IL-12 p40 after IFN-γ/LPS stimulation. Reporter gene assay, DNA affinity binding assay, endogenous mRNA induction, ICSBP-/- cell lines Journal of immunology High 10861061
2000 ICSBP expression is downregulated by BCR-ABL in CML, and forced co-expression of ICSBP inhibits BCR-ABL-induced colony formation and CML-like disease in vivo, establishing ICSBP as a tumor suppressor that counteracts BCR-ABL-driven myeloproliferation. Retroviral transduction, colony formation assay, murine bone marrow transplantation model Molecular and cellular biology High 10648600
2002 ICSBP is required for development of CD8α+ dendritic cells and mouse IFN-producing cells (plasmacytoid DC precursors) in vivo; ICSBP-/- mice lack CD8α+ DCs selectively, and this defect is intrinsic to bone marrow-derived progenitors. ICSBP-/- mouse analysis, bone marrow chimera experiments, flow cytometry, RT-PCR The Journal of experimental medicine / Blood High 12393690 12461077
2002 ICSBP's transcriptional function—requiring intact DNA-binding activity and ability to interact with partner proteins (PU.1 and other IRFs)—is essential for DC development and maturation; ICSBP mutants lacking either activity fail to rescue DC development from ICSBP-/- bone marrow. Retroviral transduction of ICSBP mutants into ICSBP-/- bone marrow, in vitro DC differentiation with Flt3 ligand Blood High 12393459
2002 Upon IFN-γ stimulation, ICSBP interacts with the Ets protein TEL at the ISRE, recruiting histone deacetylase HDAC3 to the element, causing repression of ISRE-dependent transcription as a negative-feedback mechanism; this is distinct from ICSBP-PU.1 interactions at the EICE. Mass spectrometry of ISRE-bound proteins, in vitro binding with recombinant proteins, reporter assay, co-IP Molecular and cellular biology High 12370291
2002 ICSBP and IRF-1 cooperatively stimulate murine IL-12 p40 promoter activity through a novel ISRE-like cis element (distinct from the Ets and NF-κB sites); mutation of this element abrogates ICSBP/IRF-1-driven activation. Reporter gene assay with promoter mutations, co-transfection in RAW 264.7 macrophages FEBS letters Medium 12417340
2003 NFAT physically associates with ICSBP in the absence of DNA (co-IP of endogenous proteins) and is required for ICSBP binding to the IL-12 p40 promoter; NFAT and ICSBP synergistically activate the p40 promoter, and this interaction is abrogated by IL-10. Co-immunoprecipitation of endogenous proteins, ChIP, reporter gene assay, dominant negative NFAT The Journal of biological chemistry High 12876285
2003 ICSBP inhibits growth of BCR/ABL-transformed myeloid progenitor cells by transcriptionally repressing c-Myc indirectly through direct activation of Blimp-1 and METS/PE1 (potent c-Myc repressors), without affecting BCR/ABL kinase activity. Conditional ICSBP/ER chimera expression, mRNA expression analysis, ectopic Blimp-1 expression Blood Medium 12933588
2003 ICSBP antagonizes BCR/ABL and represses bcl-2 transcription via two ICSBP-responsive elements in the bcl-2 promoter, as shown by reporter gene assays and EMSA; ICSBP overcomes BCR/ABL-induced morphology changes, chemotherapy resistance, and repression of differentiation. Reporter gene assay, EMSA, stable/conditional ICSBP expression in BCR/ABL-transformed cells Blood Medium 14656881
2003 ICSBP is critically required for development and trafficking of Langerhans cells and dermal DCs; ICSBP-/- DCs show reduced CCR6 and CCR7 expression, impaired migratory response to MIP-3α, MIP-3β, and CCL21, and failure to initiate contact hypersensitivity responses. ICSBP-/- mouse analysis, in vitro migration assay, RT-PCR for chemokine receptors, contact hypersensitivity model Blood High 14615368
2004 ICSBP/IRF-8 cooperates with PU.1 to activate transcription of the p15(Ink4b) cyclin-dependent kinase inhibitor gene; both ICSBP and PU.1 must bind DNA to form a stable complex at the p15 promoter, providing a mechanism for ICSBP tumor suppressor activity in myeloid cells. Reporter gene assay, EMSA (PU.1/ICSBP binding complex), ICSBP transduction into ICSBP-null cells Blood Medium 14976051
2005 The BXH-2 mouse carries an R294C substitution in the IRF association domain (IAD) of IRF8/ICSBP; this loss-of-function mutation impairs IL-12 production and causes myeloproliferation and immunodeficiency, confirming the IAD is essential for IRF8 function. Positional cloning, sequencing, transactivation reporter assay in RAW 264.7 macrophages The Journal of experimental medicine High 15781580
2007 The IRF8 R294C mutation (BXH2) abolishes interaction of IRF8 with partner transcription factors and prevents binding to promoters requiring partner interactions, selectively eliminating CD8α+ DC development and IL-12p40 production while retaining pDC development and type I IFN production. EMSA, chromatin immunoprecipitation (ChIP), flow cytometry of DC subsets in BXH2 mice Blood High 18055870
2007 IRF8 binds to a variant in the CHRNA1 promoter and activates CHRNA1 transcription in thymic epithelial cells; the K108E disease-associated variant prevents IRF8 binding and abrogates promoter activity, demonstrating IRF8 controls thymic promiscuous expression of a self-antigen. Promoter reporter assay in thymic epithelial cells, EMSA, in vitro mutagenesis Nature Medium 17687331
2008 IRF8 binds directly to IRF8/Ets consensus sequences in the promoters of Sfpi1 (encoding PU.1) and Ebf1, repressing Sfpi1 and activating Ebf1; a signaling-deficient IRF8 mutant fails to rescue B-cell lineage specification from IRF8-/- HSCs. ChIP, reporter gene assay, retroviral transduction of IRF8 mutants into IRF8-/- HSCs Blood High 18799728
2008 ICSBP represses PTPN13 (Fap-1) transcription via a cis element in its proximal promoter in myeloid cells; this repression is regulated by phosphorylation of conserved tyrosine residues in the IRF domain of ICSBP, and loss of ICSBP increases Fap-1, resulting in Fas dephosphorylation and apoptosis resistance. CpG island microarray ChIP screen, reporter gene assay, phosphorylation mutants, apoptosis assays The Journal of biological chemistry Medium 18195016
2007 ICSBP/IRF-8 cooperates with PU.1 and IRF-2 to activate NF1 transcription via a composite ets/IRF cis element; PU.1 binds DNA first, recruits IRF-2 (requiring phosphorylation of specific serine residues in PU.1 PEST domain and an IRF domain tyrosine in IRF-2), and ICSBP then interacts with the DNA-bound PU.1-IRF-2 heterodimer (requiring its own conserved IRF domain tyrosine). EMSA, reporter gene assay, phosphorylation mutant analysis The Journal of biological chemistry Medium 17200120
2010 ICSBP/IRF8 decreases β-catenin activity in myeloid cells by repressing GAS2 transcription (via ICSBP/Tel/HDAC3 complex at GAS2 promoter); Gas2 inhibits calpain protease, and β-catenin is a calpain substrate, so ICSBP loss elevates Gas2, inhibits calpain, and increases β-catenin protein and activity. ChIP (ICSBP/Tel/HDAC3 at GAS2 promoter), reporter gene assay, calpain activity assay, β-catenin protein quantification Molecular and cellular biology High 20679491
2011 IRF8 regulates acid ceramidase (A-CDase) expression by directly binding to its promoter; loss of IRF8 increases A-CDase protein, leading to reduced C16 ceramide and resistance to FasL-induced apoptosis in CML cells, while restoration of IRF8 suppresses CML via a Fas-dependent mechanism. ChIP (IRF8 binding to A-CDase promoter), reporter assay, ceramide measurement, apoptosis assay, in vivo CML model Cancer research High 21487040
2011 IRF8 is required for IFN-β induction in human blood monocytes by cooperating with IRF3; IRF8 constitutively binds the EICE of the IFN-β promoter together with PU.1 in vivo, forming a scaffold that facilitates recruitment of IRF3. The protein-protein interaction between IRF8 and IRF3 is independent of both the DBD of IRF8 and the IAD of IRF3. siRNA knockdown in primary monocytes, ChIP, co-IP to map interaction domains, retroviral rescue in IRF8-/- cell line Blood High 21228327
2011 IRF-8 extinguishes neutrophil production and promotes DC lineage commitment in both myeloid and lymphoid progenitors in a cell-intrinsic manner; retroviral expression of IRF-8 in GMP (which does not normally generate DCs) suppressed neutrophil production and increased DC output. Irf8-/- competitive bone marrow reconstitution, retroviral overexpression in multiple progenitor types Blood High 22238324
2011 IRF8 acts as a negative regulator of osteoclastogenesis; TLR ligands and cytokines induce IRF8 expression to inhibit osteoclast differentiation, placing IRF8 in a feedback inhibition circuit. Loss-of-function analysis in osteoclast differentiation assays, IRF8 induction by TLR ligands/cytokines Annals of the New York Academy of Sciences Low 22082370
2013 G-CSF and GM-CSF (MDSC-inducing factors) downregulate IRF-8 expression in myeloid cells via STAT3- and STAT5-dependent pathways, and IRF-8 overexpression attenuates MDSC accumulation, establishing STAT3/STAT5 as writers that suppress IRF8 to drive MDSC development. IRF-8 overexpression mouse model, Irf8-/- phenotyping, pathway analysis of STAT3/STAT5 signaling The Journal of clinical investigation Medium 24091328
2013 IRF8 and PU.1 form a complex that controls plasma cell differentiation by concurrently promoting BCL6 and PAX5 expression and repressing AID and BLIMP-1; IRF8-PU.1 complex functions reciprocally to IRF4. Genetic loss-of-function (conditional KO), reporter assay, gene expression profiling The Journal of experimental medicine Medium 25288399
2013 Wnt/β-catenin signaling activates Irf8 expression in normal hematopoiesis, and IRF8 in turn limits oncogenic β-catenin functions; combined Irf8 deletion and constitutive β-catenin activation drive CML blast crisis, establishing a cross-talk circuit. Mouse genetics (Irf8 conditional KO combined with activated β-catenin alleles), BCR-ABL CML model The Journal of experimental medicine Medium 24101380
2015 IRF8 directly activates genes involved in multiple steps of autophagy in macrophages, promotes autophagosome formation and lysosomal fusion; Irf8-/- macrophages accumulate SQSTM1 and ubiquitin-bound proteins and fail to clear Listeria monocytogenes via autophagy. Irf8-/- macrophage analysis, ChIP (IRF8 at autophagy gene promoters), autophagic flux assay, bacterial clearance assay Nature communications High 25775030
2015 Icsbp/IRF8 is required to terminate emergency granulopoiesis by repressing Fap1 and Gas2 and activating Fanconi C and F genes; loss of Icsbp results in sustained granulocyte production, resistance to Fas-induced apoptosis, increased β-catenin activity, and accelerated progression to AML. Icsbp-/- mouse emergency granulopoiesis model, gene expression analysis, apoptosis assay The Journal of biological chemistry Medium 26683374
2016 SIRT1 physically interacts with IRF8 and deacetylates it in macrophages; LPS treatment decreases SIRT1 expression and increases IRF8 expression, and LPS-induced IRF8 expression is abrogated when SIRT1 is specifically deleted. Co-immunoprecipitation, immunofluorescence, SIRT1 conditional KO macrophages Innate immunity Medium 28008797
2017 IRF8 controls Th9 differentiation through a transcription factor complex of IRF8, IRF4, PU.1, and BATF that binds DNA and activates Il9 transcription; IRF8 also dimerizes with ETV6 to repress Il4 expression. In vitro and in vivo Th9 differentiation assays (IRF8-deficient mice), ChIP, co-IP for complex components Nature communications Medium 29233972
2018 IRF8 governs the transcription of Naip genes (NLRC4 inflammasome sensors for flagellin and T3SS components) in macrophages, enabling NLRC4 inflammasome activation; IRF8 is required for optimal NLRC4 inflammasome activation against Salmonella, Burkholderia, and Pseudomonas but is dispensable for NLRP3, AIM2, and Pyrin inflammasome activation. Irf8-/- bone marrow-derived macrophages, infection assays, RNA-seq, ChIP, caspase-1 activation assay Cell High 29576451
2018 Cell-intrinsic IRF8 is required for NK cell-mediated protection against MCMV; during viral exposure, NK cells upregulate IRF8 through IL-12 signaling via STAT4, which promotes epigenetic remodeling of the Irf8 locus; IRF8 then promotes NK cell proliferation by inducing cell-cycle genes and directly controlling Zbtb32. Cell-intrinsic KO, IL-12 signaling analysis, STAT4 requirement, epigenetic analysis of Irf8 locus, MCMV infection model Immunity High 29858012
2018 Tumor-produced granulocyte-stimulating factor downregulates IRF8 in cDC progenitors, resulting in reduced cDC1 development and impaired anti-tumor CD8+ T-cell responses. Mouse tumor models (breast, pancreatic), bone marrow progenitor analysis, IRF8 expression measurement, CD8+ T-cell functional assays Nature communications Medium 29593283
2019 A +41-kb Irf8 enhancer transiently accessible in cDC1 progenitors is required for induction of Irf8 in CDPs and cDC1 fate specification; a separate +32-kb Irf8 enhancer is required for cDC1 maturation but not specification. CRISPR/Cas9 deletion of these enhancers distinguishes their roles. CRISPR/Cas9 genome editing of enhancers, chromatin profiling (ATAC-seq), in vivo DC development analysis Nature immunology High 31406378
2019 An Nfil3-Zeb2-Id2 genetic circuit controls the switch from the +41-kb to +32-kb Irf8 enhancer during cDC1 development; Nfil3 is required for the transition from Zeb2hi/Id2lo to Zeb2lo/Id2hi CDPs (earliest committed cDC1 progenitors), excluding pDC potential. Single-cell RNA sequencing of CDPs, genetic epistasis analysis (Nfil3, Zeb2, Id2 KO combinations), enhancer accessibility Nature immunology High 31406377
2019 IRF8 deletion in committed cDC1 cells (via Xcr1-Cre) causes their transcriptional, functional, and epigenetic reprogramming into cDC2-like cells, indicating IRF8 is continuously required to maintain cDC1 identity; this conversion was independent of Irf4. Xcr1-Cre conditional IRF8 deletion, RNA-seq, ATAC-seq, functional assays Immunity High 35830859
2021 ZMYND8 directly activates IRF8 through lineage-specific enhancers in AML; ZMYND8 occupancy at IRF8 enhancers requires BRD4 (a transcription coactivator), and ZMYND8 binds to the ET domain of BRD4 via its chromatin reader cassette, establishing an IRF8-MEF2D transcriptional circuit as an AML dependency. ChIP-seq (ZMYND8, BRD4, IRF8 enhancers), in vitro and in vivo ZMYND8 KO, protein interaction mapping Molecular cell High 34358447
2021 A RUNX-CBFβ-driven enhancer 56 kb downstream of the Irf8 transcription start site controls Irf8 expression throughout the myeloid lineage; deletion of this enhancer decreases IRF8 throughout myeloid progenitors, resulting in loss of cDC progenitors and overproduction of Ly6C+ monocytes, and demonstrates that IRF8 expression level (high/low/null) dose-dependently directs cDC1/monocyte/neutrophil fate via distinct sets of enhancers. In vivo CRISPR enhancer deletion, scRNA-seq, ATAC-seq, flow cytometric lineage analysis Nature immunology High 33603226
2021 Brd4 forms a complex with IRF8/PU.1 and binds to IRF8 and PU.1 binding motifs on Naip promoters to maintain Naip expression; Brd4-deficient macrophages show impaired NLRC4 inflammasome activation and reduced Naip transcription. Co-IP (Brd4/IRF8/PU.1 complex), ChIP, Brd4-/- macrophage infection assay, RNA-seq The Journal of cell biology High 33535228
2022 IRF8 promotes STING-mediated innate immune responses in monocytes through a transcription-independent mechanism: in uninfected cells IRF8 is inactive (IAD sequestered by N- and C-terminal tails); upon cGAS-STING pathway activation, IRF8 is phosphorylated at Serine 151, enabling its IRF-association domain to bind STING, promoting STING polymerization and TBK1-mediated phosphorylation of STING and IRF3. Phospho-mutant analysis, co-IP, IRF8-deficient monocytes, HSV-1 infection model, STING polymerization assay Nature communications High 35973990
2022 TAM-specific IRF8 is required for tumor-associated macrophages to present cancer cell antigens and promote CTL exhaustion in tumors; TAM-specific IRF8 deletion prevented exhaustion of cancer-reactive CTLs and suppressed tumor growth. TAM-specific conditional IRF8 deletion, antigen presentation assays, CTL exhaustion markers, tumor growth assay Immunity High 36288724
2022 IRF8 suppresses T-ALL by inhibiting the PI3K/AKT signaling pathway; FTO (m6A demethylase) binds to m6A sites in the 3' UTR of IRF8 mRNA and promotes its degradation, silencing IRF8 in T-ALL cells. IRF8 overexpression/KO in T-ALL cells, PI3K/AKT signaling analysis, m6A-seq, RIP-seq (FTO binding to IRF8 mRNA), FTO inhibition in vivo Advanced science Medium 36478193
2024 IRF8 binds stepwise to enhancer regions in postnatal microglia together with Sall1 and PU.1, reaching maximum binding after day 14; IRF8 binding correlates with stepwise increases in chromatin accessibility preceding microglial-specific transcriptome initiation; IRF8 is also required for microglial-specific DNA methylation patterns. Constitutive or postnatal Irf8 deletion causes loss of microglial identity and gain of disease-associated microglia (DAM)-like gene expression. ChIP-seq, ATAC-seq, scRNA-seq, scATAC-seq, conditional Irf8 deletion (constitutive and postnatal), bisulfite sequencing (DNA methylation), 5xFAD model Nature immunology High 39313544
2020 IRF8 deficiency causes cDC2 heterogeneity through two distinct pathways: a lymphoid-primed IRF8hi pathway (marked by CD123 and BTLA) carries pDC, cDC1, and DC2 trajectories, while a common myeloid IRF8lo pathway (SIRPA+) generates DC3s and monocytes; DC3s expand to replace DC2s in human partial IRF8 deficiency. Human IRF8-deficiency allelic series, high-dimensional flow cytometry, in vitro differentiation from human stem cells Immunity High 32735845
2018 IRF8 promotes NLRP3 inflammasome activation during Gram-negative bacterial infection by mediating phosphorylation of IRF3, which is required for Ifnb transcription; IFN-β in turn triggers caspase-11-dependent NLRP3 inflammasome activation. IRF8 was previously shown to be dispensable for caspase-11-mediated NLRP3 activation during LPS transfection. IRF8-/- bone marrow-derived macrophages, caspase-1/caspase-11 activation assays, Gram-negative bacterial infection, IRF3 phosphorylation analysis Journal of immunology Medium 32205422
2019 IRF8 inhibits osteoclastogenesis; an IRF8 G388S mutation promotes osteoclastogenesis and fails to inhibit NFATc1-dependent transcriptional activation; IRF8 constitutively binds regulatory regions of thousands of genes in osteoclast precursors and its loss enhances osteoclast-specific transcripts. Functional osteoclastogenesis assay, NFATc1 reporter assay, ChIP-seq in osteoclast precursors, Irf8+/- mouse alveolar bone analysis Journal of bone and mineral research High 30840779
2021 PU.1 and IRF8 bind to an Ets/IRF composite element (EICE) in the distal promoter of human NLRP3, controlling its monocytic lineage-specific expression; knockdown of PU.1 and/or IRF8 downregulates NLRP3 expression and markedly diminishes LPS-induced IL-1β release. Reporter assay, EMSA, ChIP, siRNA knockdown in THP-1 and primary macrophages Frontiers in immunology Medium 33897697
2018 IRF8 and PU.1 are required for microglial activation; both factors directly target each other's gene transcription in a positive feedback loop; IRF8 and PU.1 cooperatively bind composite IRF-ETS motifs on microglial activation-related genes, verified biochemically by synergistic binding to composite-motif DNA. Post-developmental conditional deletion in microglia, 3D fluorescence imaging, ChIP, biochemical DNA-binding assay Protein & cell Medium 30484118
2012 miR-22 directly targets the 3' UTR of Irf8 mRNA for post-transcriptional repression, controlling DC subset differentiation; miR-22 overexpression enhanced cDC generation at the expense of pDCs while reducing Irf8 mRNA abundance. Luciferase reporter assay (miR-22 binding Irf8 3' UTR), miR-22 overexpression/knockdown during DC development PloS one Medium 23251709

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1996 Immunodeficiency and chronic myelogenous leukemia-like syndrome in mice with a targeted mutation of the ICSBP gene. Cell 563 8861914
2011 IRF8 mutations and human dendritic-cell immunodeficiency. The New England journal of medicine 470 21524210
2002 ICSBP is essential for the development of mouse type I interferon-producing cells and for the generation and activation of CD8alpha(+) dendritic cells. The Journal of experimental medicine 337 12461077
2013 Myeloid-derived suppressor cell development is regulated by a STAT/IRF-8 axis. The Journal of clinical investigation 288 24091328
2000 ICSBP directs bipotential myeloid progenitor cells to differentiate into mature macrophages. Immunity 254 10981959
2002 Essential role for ICSBP in the in vivo development of murine CD8alpha + dendritic cells. Blood 252 12393690
2020 Differential IRF8 Transcription Factor Requirement Defines Two Pathways of Dendritic Cell Development in Humans. Immunity 201 32735845
2018 Breast and pancreatic cancer interrupt IRF8-dependent dendritic cell development to overcome immune surveillance. Nature communications 190 29593283
1993 The genomic structure of the murine ICSBP gene reveals the presence of the gamma interferon-responsive element, to which an ISGF3 alpha subunit (or similar) molecule binds. Molecular and cellular biology 185 8321202
1998 Lack of interferon consensus sequence binding protein (ICSBP) transcripts in human myeloid leukemias. Blood 171 9414265
2002 ICSBP/IRF-8: its regulatory roles in the development of myeloid cells. Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research 164 11846985
2022 Tumor-associated macrophages expressing the transcription factor IRF8 promote T cell exhaustion in cancer. Immunity 161 36288724
2018 IRF8 Regulates Transcription of Naips for NLRC4 Inflammasome Activation. Cell 160 29576451
2019 Cryptic activation of an Irf8 enhancer governs cDC1 fate specification. Nature immunology 154 31406378
2000 An IFN-gamma-inducible transcription factor, IFN consensus sequence binding protein (ICSBP), stimulates IL-12 p40 expression in macrophages. Journal of immunology (Baltimore, Md. : 1950) 151 10861061
2007 An IRF8-binding promoter variant and AIRE control CHRNA1 promiscuous expression in thymus. Nature 148 17687331
2007 The BXH2 mutation in IRF8 differentially impairs dendritic cell subset development in the mouse. Blood 140 18055870
2012 IRF-8 extinguishes neutrophil production and promotes dendritic cell lineage commitment in both myeloid and lymphoid mouse progenitors. Blood 123 22238324
2014 The transcription factors IRF8 and PU.1 negatively regulate plasma cell differentiation. The Journal of experimental medicine 122 25288399
2008 IRF8 regulates B-cell lineage specification, commitment, and differentiation. Blood 120 18799728
2000 Expression of interferon consensus sequence binding protein (ICSBP) is downregulated in Bcr-Abl-induced murine chronic myelogenous leukemia-like disease, and forced coexpression of ICSBP inhibits Bcr-Abl-induced myeloproliferative disorder. Molecular and cellular biology 116 10648600
2018 Transcription Factor IRF8 Orchestrates the Adaptive Natural Killer Cell Response. Immunity 108 29858012
2009 IRF8 regulates myeloid and B lymphoid lineage diversification. Immunologic research 105 18806934
2015 Regulation of myelopoiesis by the transcription factor IRF8. International journal of hematology 102 25749660
1995 Functional domain analysis of interferon consensus sequence binding protein (ICSBP) and its association with interferon regulatory factors. The Journal of biological chemistry 99 7768900
2019 An Nfil3-Zeb2-Id2 pathway imposes Irf8 enhancer switching during cDC1 development. Nature immunology 97 31406377
2020 Role of IRF8 in immune cells functions, protection against infections, and susceptibility to inflammatory diseases. Human genetics 94 32232558
2002 ICSBP/IRF-8 retrovirus transduction rescues dendritic cell development in vitro. Blood 93 12393459
2016 Biallelic mutations in IRF8 impair human NK cell maturation and function. The Journal of clinical investigation 88 27893462
2005 A mutation in the Icsbp1 gene causes susceptibility to infection and a chronic myeloid leukemia-like syndrome in BXH-2 mice. The Journal of experimental medicine 86 15781580
2003 ICSBP is critically involved in the normal development and trafficking of Langerhans cells and dermal dendritic cells. Blood 85 14615368
2011 Shared and distinct functions of the transcription factors IRF4 and IRF8 in myeloid cell development. PloS one 82 22003407
2003 Activation of the murine interleukin-12 p40 promoter by functional interactions between NFAT and ICSBP. The Journal of biological chemistry 82 12876285
2003 Interferon consensus sequence binding protein (ICSBP; IRF-8) antagonizes BCR/ABL and down-regulates bcl-2. Blood 78 14656881
2019 Transcription factors IRF8 and PU.1 are required for follicular B cell development and BCL6-driven germinal center responses. Proceedings of the National Academy of Sciences of the United States of America 71 31000603
2002 IRF-8/ICSBP and IRF-1 cooperatively stimulate mouse IL-12 promoter activity in macrophages. FEBS letters 69 12417340
2006 Identification of IRF-8 and IRF-1 target genes in activated macrophages. Molecular immunology 68 16597464
2018 Transcriptional mechanism of IRF8 and PU.1 governs microglial activation in neurodegenerative condition. Protein & cell 67 30484118
2015 IRF8 directs stress-induced autophagy in macrophages and promotes clearance of Listeria monocytogenes. Nature communications 67 25775030
2011 IRF8 and IRF3 cooperatively regulate rapid interferon-β induction in human blood monocytes. Blood 67 21228327
2002 ICSBP/IRF-8 transactivation: a tale of protein-protein interaction. Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research 66 11846986
2011 IRF8 regulates acid ceramidase expression to mediate apoptosis and suppresses myelogeneous leukemia. Cancer research 61 21487040
2002 Gamma interferon triggers interaction between ICSBP (IRF-8) and TEL, recruiting the histone deacetylase HDAC3 to the interferon-responsive element. Molecular and cellular biology 61 12370291
2017 Modelling IRF8 Deficient Human Hematopoiesis and Dendritic Cell Development with Engineered iPS Cells. Stem cells (Dayton, Ohio) 58 28090699
2002 Disabled-2 is transcriptionally regulated by ICSBP and augments macrophage spreading and adhesion. The EMBO journal 56 11823414
2017 IRF8-dependent molecular complexes control the Th9 transcriptional program. Nature communications 55 29233972
2021 ZMYND8-regulated IRF8 transcription axis is an acute myeloid leukemia dependency. Molecular cell 54 34358447
2021 A RUNX-CBFβ-driven enhancer directs the Irf8 dose-dependent lineage choice between DCs and monocytes. Nature immunology 53 33603226
2003 ICSBP/IRF-8 inhibits mitogenic activity of p210 Bcr/Abl in differentiating myeloid progenitor cells. Blood 53 12933588
2022 IRF8 deficiency induces the transcriptional, functional, and epigenetic reprogramming of cDC1 into the cDC2 lineage. Immunity 52 35830859
2016 PU.1 cooperates with IRF4 and IRF8 to suppress pre-B-cell leukemia. Leukemia 52 26932576
2008 The interferon consensus sequence-binding protein (ICSBP/IRF8) represses PTPN13 gene transcription in differentiating myeloid cells. The Journal of biological chemistry 52 18195016
2007 PU.1, interferon regulatory factor (IRF) 2, and the interferon consensus sequence-binding protein (ICSBP/IRF8) cooperate to activate NF1 transcription in differentiating myeloid cells. The Journal of biological chemistry 51 17200120
2020 Suppression of Inflammasome Activation by IRF8 and IRF4 in cDCs Is Critical for T Cell Priming. Cell reports 50 32375053
2004 The interferon regulatory factor ICSBP/IRF-8 in combination with PU.1 up-regulates expression of tumor suppressor p15(Ink4b) in murine myeloid cells. Blood 50 14976051
2022 IRF8: Mechanism of Action and Health Implications. Cells 48 36078039
2020 IRF3 and IRF8 Regulate NF-κB Signaling by Targeting MyD88 in Teleost Fish. Frontiers in immunology 47 32373114
2019 Leukocyte-specific siRNA delivery revealing IRF8 as a potential anti-inflammatory target. Journal of controlled release : official journal of the Controlled Release Society 46 31634546
2013 Genetic variation near IRF8 is associated with serologic and cytokine profiles in systemic lupus erythematosus and multiple sclerosis. Genes and immunity 45 23965942
2013 Cross talk between Wnt/β-catenin and Irf8 in leukemia progression and drug resistance. The Journal of experimental medicine 45 24101380
2022 Transcription-independent regulation of STING activation and innate immune responses by IRF8 in monocytes. Nature communications 44 35973990
2020 CD163 expression defines specific, IRF8-dependent, immune-modulatory macrophages in the bone marrow. The Journal of allergy and clinical immunology 44 32199911
2014 IRF4 and IRF8: Governing the virtues of B Lymphocytes. Frontiers in biology 44 25506356
2010 Interferon consensus sequence binding protein (ICSBP) decreases beta-catenin activity in myeloid cells by repressing GAS2 transcription. Molecular and cellular biology 44 20679491
2006 Interferon-gamma induces regression of epithelial cell carcinoma: critical roles of IRF-1 and ICSBP transcription factors. Oncogene 43 16462767
1994 IFN consensus sequence binding protein (ICSBP) is a conditional repressor of IFN inducible promoters. International immunology 42 7526889
2007 Icsbp1/IRF-8 is required for innate and adaptive immune responses against intracellular pathogens. Journal of immunology (Baltimore, Md. : 1950) 41 17675508
2015 Transcription factor IRF8 controls Th1-like regulatory T-cell function. Cellular & molecular immunology 40 26166768
1995 Chicken interferon consensus sequence-binding protein (ICSBP) and interferon regulatory factor (IRF) 1 genes reveal evolutionary conservation in the IRF gene family. Proceedings of the National Academy of Sciences of the United States of America 38 7536924
2008 IFN consensus sequence binding protein (Icsbp) is critical for eosinophil development. Journal of immunology (Baltimore, Md. : 1950) 37 18802108
2015 STAT1 and IRF8 in Vascular Inflammation and Cardiovascular Disease: Diagnostic and Therapeutic Potential. International reviews of immunology 36 26606328
2008 Expression of the interferon regulatory factor 8/ICSBP-1 in human reactive lymphoid tissues and B-cell lymphomas: a novel germinal center marker. The American journal of surgical pathology 35 18580679
2008 Epigenetic silencing of the interferon regulatory factor ICSBP/IRF8 in human multiple myeloma. Experimental hematology 35 18922617
2016 IRF8 is the target of SIRT1 for the inflammation response in macrophages. Innate immunity 33 28008797
2021 Brd4 regulates NLRC4 inflammasome activation by facilitating IRF8-mediated transcription of Naips. The Journal of cell biology 32 33535228
2012 miR-22 controls Irf8 mRNA abundance and murine dendritic cell development. PloS one 32 23251709
2010 Cooperation between deficiencies of IRF-4 and IRF-8 promotes both myeloid and lymphoid tumorigenesis. Blood 32 20585039
2022 Lupus enhancer risk variant causes dysregulation of IRF8 through cooperative lncRNA and DNA methylation machinery. Nature communications 31 35388006
2014 Interferon consensus sequence-binding protein (ICSBP) promotes epithelial-to-mesenchymal transition (EMT)-like phenomena, cell-motility, and invasion via TGF-β signaling in U2OS cells. Cell death & disease 31 24832596
2013 Batf3 and Id2 have a synergistic effect on Irf8-directed classical CD8α+ dendritic cell development. Journal of immunology (Baltimore, Md. : 1950) 31 24227775
2020 IRF8 Regulates Gram-Negative Bacteria-Mediated NLRP3 Inflammasome Activation and Cell Death. Journal of immunology (Baltimore, Md. : 1950) 30 32205422
2019 Inactivating Mutation in IRF8 Promotes Osteoclast Transcriptional Programs and Increases Susceptibility to Tooth Root Resorption. Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research 30 30840779
2024 IRF8 defines the epigenetic landscape in postnatal microglia, thereby directing their transcriptome programs. Nature immunology 29 39313544
2022 IL-10 inhibits osteoclast differentiation and osteolysis through MEG3/IRF8 pathway. Cellular signalling 28 35525407
1999 Interferon-gamma signaling in human retinal pigment epithelial cells mediated by STAT1, ICSBP, and IRF-1 transcription factors. Investigative ophthalmology & visual science 26 10102295
2014 Constitutive IRF8 expression inhibits AML by activation of repressed immune response signaling. Leukemia 25 24957708
2011 Feedback inhibition of osteoclastogenesis during inflammation by IL-10, M-CSF receptor shedding, and induction of IRF8. Annals of the New York Academy of Sciences 25 22082370
2009 ICSBP-mediated immune protection against BCR-ABL-induced leukemia requires the CCL6 and CCL9 chemokines. Blood 25 19171873
2022 Host Cells Actively Resist Porcine Reproductive and Respiratory Syndrome Virus Infection via the IRF8-MicroRNA-10a-SRP14 Regulatory Pathway. Journal of virology 24 35293774
2013 IRF5, IRF8, and IRF7 in human pDCs - the good, the bad, and the insignificant? European journal of immunology 24 23828296
2022 Silencing of IRF8 Mediated by m6A Modification Promotes the Progression of T-Cell Acute Lymphoblastic Leukemia. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 23 36478193
2021 High IRF8 expression correlates with CD8 T cell infiltration and is a predictive biomarker of therapy response in ER-negative breast cancer. Breast cancer research : BCR 23 33766090
2021 IRF-8/miR-451a regulates M-MDSC differentiation via the AMPK/mTOR signal pathway during lupus development. Cell death discovery 23 34282122
2021 PU.1 and IRF8 Modulate Activation of NLRP3 Inflammasome via Regulating Its Expression in Human Macrophages. Frontiers in immunology 22 33897697
2008 Decreased IRF8 expression found in aging hematopoietic progenitor/stem cells. Leukemia 22 18596738
2006 ICSBP/IRF-8 differentially regulates antigen uptake during dendritic-cell development and affects antigen presentation to CD4+ T cells. Blood 22 16569763
2015 Association of IRF8 gene polymorphisms with autoimmune thyroid disease. European journal of clinical investigation 20 25989711
2015 The Interferon Consensus Sequence Binding Protein (Icsbp/Irf8) Is Required for Termination of Emergency Granulopoiesis. The Journal of biological chemistry 20 26683374
2017 IRF-8 is Involved in Amyloid-β1-40 (Aβ1-40)-induced Microglial Activation: a New Implication in Alzheimer's Disease. Journal of molecular neuroscience : MN 19 28856571
2013 A role for IRF8 in B cell anergy. Journal of immunology (Baltimore, Md. : 1950) 19 24218455

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