ArticleJournal of immunology (Baltimore, Md. : 1950)2012
Monocytes from Irf5-/- mice have an intrinsic defect in their response to pristane-induced lupus.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 55 citations in OpenAlex.
- Inhibition of IRF5 hyperactivation protects from lupus onset and severity.The Journal of clinical investigation · 2020Trial
- The role of IRF5 as an immune regulator.Biochemical Society transactions · 2026Review
- Escape of Kdm6a from X Chromosome Is Detrimental to Ischemic Brains via IRF5 Signaling.Translational stroke research · 2025Article
- IRF5 Controls Plasma Cell Generation and Antibody Production via Distinct Mechanisms Depending on the Antigenic Trigger.Immunology · 2025Article
- Escape of Kdm6a from X chromosome is detrimental to ischemic brains via IRF5 signaling.Research square · 2024Article
- IRF5 governs macrophage adventitial infiltration to fuel abdominal aortic aneurysm formation.JCI insight · 2024Article
- Loss of NOD2 in macrophages improves colitis and tumorigenesis in a lysozyme-dependent manner.Frontiers in immunology · 2023Article
- A phospho-tyrosine-based signaling module using SPOP, CSK, and LYN controls TLR-induced IRF activity.Science advances · 2022Article
- Involvement of MST1/mTORC1/STAT1 activity in the regulation of B-cell receptor signalling by chemokine receptor 2.Clinical and translational medicine · 2022Article
- Defactinib inhibits PYK2 phosphorylation of IRF5 and reduces intestinal inflammation.Nature communications · 2021Article
- A catalog of GWAS fine-mapping efforts in autoimmune disease.American journal of human genetics · 2021Review
- Monocytopenia, monocyte morphological anomalies and hyperinflammation characterise severe COVID-19 in type 2 diabetes.EMBO molecular medicine · 2020Observational
- Coordination between innate immune cells, type I IFNs and IRF5 drives SLE pathogenesis.Cytokine · 2020Review
- T Cell-Intrinsic IRF5 Regulates T Cell Signaling, Migration, and Differentiation and Promotes Intestinal Inflammation.Cell reports · 2020Article
- IRF5 guides monocytes toward an inflammatory CD11cScience immunology · 2020Article
- Inhibition of IRF5 cellular activity with cell-penetrating peptides that target homodimerization.Science advances · 2020Article
- Antibody response to homologous epitopes of Epstein-Barr virus,Journal of translational autoimmunity · 2020Article
- Reducing IRF5 expression attenuates colitis in mice, but impairs the clearance of intestinal pathogens.Mucosal immunology · 2019Article
- Irf5 deficiency in myeloid cells prevents necrotizing enterocolitis by inhibiting M1 macrophage polarization.Mucosal immunology · 2019Article
- Genetic Versus Non-genetic Drivers of SLE: Implications of IRF5 Dysregulation in Both Roads Leading to SLE.Current rheumatology reports · 2019Review
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
The transcription factor IFN regulatory factor (IRF)5 has been identified as a human systemic lupus erythematosus (SLE) susceptibility gene by numerous joint linkage and genome-wide association studies. Although IRF5 expression is significantly elevated in primary blood cells of SLE patients, it is not yet known how IRF5 contributes to SLE pathogenesis. Recent data from mouse models of lupus indicate a critical role for IRF5 in the production of pathogenic autoantibodies and the expression of Th2 cytokines and type I IFN. In the present study, we examined the mechanisms by which loss of Irf5 protects mice from pristane-induced lupus at early time points of disease development. We demonstrate that Irf5 is required for Ly6C(hi) monocyte trafficking to the peritoneal cavity, which is thought to be one of the initial key events leading to lupus pathogenesis in this model. Chemotaxis assays using peritoneal lavage from pristane-injected Irf5(+/+) and Irf5(-/-) littermates support an intrinsic defect in Irf5(-/-) monocytes. We found the expression of chemokine receptors CXCR4 and CCR2 to be dysregulated on Irf5(-/-) monocytes and less responsive to their respective ligands, CXCL12 and CCL2. Bone marrow reconstitution experiments further supported an intrinsic defect in Irf5(-/-) monocytes because Irf5(+/+) monocytes were preferentially recruited to the peritoneal cavity in response to pristane. Taken together, these findings demonstrate an intrinsic role for IRF5 in the response of monocytes to pristane and their recruitment to the primary site of inflammation that is thought to trigger lupus onset in this experimental model of SLE.
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