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.

Functional assays in LUAD cells and macrophages treated with the TLR8 agonist Motolimod examined proliferation, migration, invasion, phagocytosis, mitochondrial activity, and ROS generation...Mechanistically, TLR8 activation in macrophages was associated with reduced mitochondrial membrane potential, increased ROS production, and the acquisition of an M1-like, antitumor phenotype with enhanced phagocytosis and cytokine secretion. TLRscore is a novel biomarker for prognosis and immunotherapy response, while TLR8 represents a promising therapeutic target in LUAD, providing mechanistic insight into potential combination strategies.

P1/2, N=320, Active, not recruiting, Ascendis Pharma Oncology Division A/S | Recruiting --> Active, not recruiting

P1/2, N=75, Recruiting, SURGE Therapeutics | Trial completion date: Dec 2025 --> Aug 2026 | Trial primary completion date: Dec 2025 --> May 2026

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.

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.

P4, N=60, Not yet recruiting, China-Japan Friendship Hospital; China-Japan Friendship Hospital

P2, N=45, Not yet recruiting, The first affiliated hostipal of nanchang university; The first affiliated hostipal of nanchang university

P1, N=117, Active, not recruiting, M.D. Anderson Cancer Center | Enrolling by invitation --> Active, not recruiting

Both imiquimod and gardiquimod treatment inhibited tumor growth, with gardiquimod showing an increased potency compared to imiquimod. This implies that TLR agonists like imiquimod and gardiquimod could serve as neoadjuvant, adjuvant, or complementary immunotherapeutic agents in melanoma therapy.