The validation confirmed that this model is capable of directly detecting Poly(I:C) -induced transient IFNγ, enhancing intratumoral IFNγ signals upon anti-PD-1/CTLA-4 therapy, and dynamically tracking IFNγ expression during imiquimod-induced psoriasis. This transgenic mouse model provides a powerful tool for non-invasive, longitudinal tracking of IFNγ-expressing cells, offering novel insights into IFNγ-mediated immune regulation in inflammation and cancer. It holds promise for identifying IFNγ-related therapeutic targets and predicting responses to immunotherapies.
Non-surgical modalities-including photodynamic therapy, topical imiquimod, radiotherapy and, in advanced disease, systemic chemotherapy, HER2 targeted agents and immune checkpoint inhibitors-provide additional options in selected patients. A multidisciplinary, biomarker driven approach is essential to individualize management and improve long-term outcomes in this challenging disease.
Our findings indicate that Grg3 confers protective effects in a murine model of imiquimod-induced psoriasis-like dermatitis. The potential therapeutic properties of Grg3 potentially involve modulation of NLRP3 inflammasome activation, suppression of NF-κB signaling, and restoration of Th17/Treg cell homeostasis.
This study investigated the individual and combinatorial effects of TLR3 Poly(I:C), TLR5 (Flagellin), and TLR7 (Imiquimod) ligands on nitric oxide (NO) production and pro-inflammatory cytokine expression in RAW 264.7 mouse macrophage cells...These findings highlight a potent crosstalk between TRIF-dependent (TLR3) and MyD88-dependent (TLR7, TLR5) signaling pathways, leading to amplified immune activation. Our study highlights the potential of synergistic TLR ligand combinations as powerful immunomodulators, offering promising avenues for the rational design of more effective vaccine adjuvants and innovative strategies in cancer immunotherapy.
25 days ago
Journal • IO biomarker
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MYD88 (MYD88 Innate Immune Signal Transduction Adaptor) • IFNG (Interferon, gamma) • IL6 (Interleukin 6) • TNFA (Tumor Necrosis Factor-Alpha) • TLR3 (Toll Like Receptor 3) • TLR5 (Toll Like Receptor 5) • TLR7 (Toll Like Receptor 7)
Using CRISPR/Cas9 to generate S100a4 gene knockout mice, imiquimod was continuously applied to the back skin to induce the psoriasis disease model...Our findings suggest a potential pathogenic role for S100A4 in psoriasis and highlight previously uncharacterized cell-specific transcriptional landscapes and regulatory mechanisms. Our results provide novel insights into the complex pathology of psoriasis and could offer important clues for the development of new targeted therapeutic strategies.