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November 1, 2025The Journal of ImmunologyOpen Access

IRF5 is required for iHPC differentiation in a mouse model of TLR7-driven macrophage activation syndrome and inhibition of IRF5 activity rescues from disease severity 3604

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Authors

ALAiling LuNTNatalie K ThulinAHAmanda Huang

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Overview

Inhibition of irf5 reduces disease severity in mice with macrophage activation syndrome, indicating a potential treatment strategy.

Key Points

  • This research investigates the role of irf5 in the differentiation of inflammatory hemophagocytes in macrophage activation syndrome.
  • Generated TLR7.1/Irf5+/- and TLR7.1Irf5-/- mouse models
  • Utilized the irf5 inhibitor (N5-1) in the TLR7.1 MAS model
  • Examined iHPC generation and hemophagocytosis by flow cytometry and immunofluorescence
  • Administered N5-1 in preclinical and therapeutic dosing regimens
  • N5-1 partially inhibits iHPC generation and prevents hemophagocytosis
  • N5-1 alleviates symptoms of MAS in TLR7.1 mice
  • Irf5 deficiency in TLR7.1 mice significantly rescues the MAS phenotype

Cite This Study

Lu et al. (2025) studied this question.

synapsesocial.com/papers/69254f89c0ce034ddc359757https://doi.org/10.1093/jimmun/vkaf283.1384
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1IRF5 is required for inflammatory hemophagocyte differentiation and disease development in TLR7-mediated Macrophage Activation Syndrome 46432025
  2. 2GM-CSF-IRF5 Axis as a Therapeutic Target in TLR7-Mediated Macrophage Activation Syndrome 23091922026
  3. 3IRF5 governs liver macrophage activation that promotes hepatic fibrosis in mice and humans2016 · 65 citations
  4. 4IRF5 mediates adaptive immunity via altered glutamine metabolism, mTORC1 signaling and post-transcriptional regulation following T cell receptor activation 28972025
  5. 5Liver type 1 innate lymphoid cells undergo apoptosis in murine models of macrophage activation syndrome and are dispensable for disease2024 · 3 citations