IRF5 promotes inflammatory macrophage polarization and TH1-TH17 responses

By Thomas Krausgruber, K. Blazek, T. Smallie, S. Alzabin, H. Lockstone, N. Sahgal, T. Hussell, M. Feldmann, I. Udalova. Nature Immunology, 2011

1,305 citations recorded by the source corpus.

Subfields: Immunology

View Paper: https://www.semanticscholar.org/paper/9189f287d71a86c4f5891b488b6ec7fdfe8437cb

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In Immunology

1. A. Mantovani
2. F. Martínez
3. P. Allavena
4. S. Gordon
5. R. Locksley
6. L. Chávez-Galán
7. I. Garcia
8. D. Vesin

Citations in the corpus

• The interaction of anticancer therapies with tumor-associated macrophages (2015, background): “Transcription factors involved in M1 polarization include NF-B, STAT1, and IRF5 (Krausgruber et al., 2011), whereas IRF4, STAT6, MYC, and, secondarily, PPAR and KLF4 have been associated with M2 polarization (Sica and Mantovani, 2012; Murray et al., 2014).”
• Macrophages in immunoregulation and therapeutics (2023, background): “IRF-5 can directly recruit to M1 gene promoters such as Il12b, whereas it represses transcription of M2 marker Il10.”
• Macrophage Polarization: Different Gene Signatures in M1(LPS+) vs. Classically and M2(LPS–) vs. Alternatively Activated Macrophages (2019, background): “IL-23a drives inflammation through the induction of IL-17, promoting a highly pro-inflammatory Th17 response (44).”
• Overview of General and Discriminating Markers of Differential Microglia Phenotypes (2020, background): “M1 activation of microglia is considered as aggressive, leading to cytotoxicity and robust, immediate inflammation related to the release of pro-inflammatory cytokines and chemokines (e.g., TNFα, IL-6, IL-1β).”
• Dual Roles of Immune Cells and Their Factors in Cancer Development and Progression (2011, background): “It has been shown that these conditions promote IRF5 expression in macrophages, leading to production and maintenance of M1 phenotypic markers and encouraging lymphocyte proliferation and Th1/Th17 cellular responses by directly up-regulating the transcription of IL-12p35, IL-12p40, IL-23 and TNF-α (”
• Macrophage Polarization in Inflammatory Diseases (2014, background): “Many key transcription factors are involved in macrophage polarization[12], like signal transducer and activator of transcription (STATs)[13], interferon-regulatory factor (IRFs)[14, 15], nuclear factor (NF)-κB [16], activator protein (AP) 1 [17], peroxisome proliferator-activated receptor (PPAR)-γ ”
• Molecular Mechanisms That Influence the Macrophage M1–M2 Polarization Balance (2014, background): “IL-4 induces not only c-Myc, which controls the expression of a subset of M2-associated genes but also the M2-polarizing IRF-4 axis to inhibit IRF5-mediated M1 polarization.”
• The M1 and M2 paradigm of macrophage activation: time for reassessment (2014, background): “forms a dodecamer structure [34] and recruits JAK2, leading to the activation of STAT5, extracellular signal-regulated kinase (ERK), and V-Akt murine thymoma viral oncogene homolog 1 (AKT) as well as the nuclear translocation of NF-kB and IRF5 upon binding (Figure 1B) [35].”