clodronate disodium

IFNG+IL17+CD4+ T cells and CXCL9/10-producing macrophages are key mediators of irColitis. Targeting IL-23 signaling and intestinal macrophages represents a promising strategy to alleviate gut immunopathology without compromising the efficacy of ICB therapy.

TAMs, particularly M1-like subsets, play a critical role in mediating resistance to OVM therapy by reducing viral persistence and suppressing CD8+ T-cell responses. Targeting TAMs significantly improves the antitumor efficacy of OVM in solid tumors. These findings support the development of TAMs-targeted combination strategies to optimize oncolytic virotherapy.

Clodronate liposomes were used to reduce circulating monocytes in vivo...Endothelial RIPK3 suppresses EC activation and inflammation associated with IL-6 and VCAM-1 elevation to protect the vascular barrier in the context of intestinal I/R injury. Thus, endothelial RIPK3 plays surprisingly beneficial roles that reduce I/R injury-induced vascular dysfunction.

We demonstrate unique metabolic dependency of β-catenin-mutated HCCs on GS in tumor cells which is diverted to macrophages upon GS elimination in tumor cells. This adaptation alters macrophage metabolism and function leading to compromised immunosurveillance and greater tumor burden. Our study reveals a metabolic dynamic between HCC cells and macrophages with impact on tumor biology.

To distinguish PET signals from tumor cells versus macrophages, immunocompetent C57BL/6 mice bearing syngeneic TRAMP-C2 prostate tumors were divided into three cohorts and treated with PBS (control), cold anti-B7-H4 mAb (for B7-H4 blockade), or clodronate liposome (for macrophage depletion)...Collectively, these results show that [89Zr]Zr-DFO-2H9 binds B7-H4 with high affinity and specificity and reflects changes in TAM levels in vivo. The new radiotracer shows promise for detecting B7-H4 positive tumors and TAM levels, profiling the immune microenvironment, and monitoring macrophage-targeted immunotherapies.

A lung metastatic colon cancer model was established via intravenous injection of CT26-luciferase cells and then treated with Lipo-Re188 (11.1 MBq, 30% of MTD), liposomal clodronate (Lipo-clod) for macrophage depletion, and/or anti-PD-L1 antibody...Our study reveals that triple therapy overcomes immunosuppressive feedback and promotes a tumor-suppressive microenvironment. These findings support a rational combination strategy integrating radiopharmaceutical therapy with immune modulation for metastatic cancer treatment.

This study provides evidence that ICS II exerts significant anti-inflammatory and neuroprotective effects. This is achieved by inhibiting the cGAS-STING pathway and suppressing macrophage M1 polarization, suggesting its potential as a therapeutic agent for STC.

P3, N=24, Recruiting, Sunnybrook Health Sciences Centre | Not yet recruiting --> Recruiting | Trial completion date: Nov 2025 --> Dec 2027 | Trial primary completion date: Oct 2025 --> Dec 2027

[METHODS]: We studied K19-Wnt1/C2mE mice fed HFD or control diet with or without systemic administration of Escherichia coli LPS ± clodronate liposomes (CLs)...LPS stimulation of MKN7 cells increased the expression of NQO1, phosphorylated NFκB and PD-L1, and NRF2 directly regulated CD274 transcription. [CONCLUSIONS]: HFD-related metabolic endotoxemia may promote GCA progression via PD-L1 induction in tumor cells directly through Nrf2 signaling activated by LPS and through NFκB signaling by TNF-α from LPS-activated macrophages in tumor microenvironment.

The anti-tumor effects of DB2313 were abolished by depleting macrophages with clodronate or inhibiting the CXCL9-CXCR3 chemokine axis using CXCL9- or CXCR3-neutralizing antibodies. These results suggest that pharmacological inhibition of PU.1 suppresses tumor growth by at least promoting the infiltration of lymphocytes into tumors through the CXCL9-CXCR3 chemokine axis. Our study establishes a framework for developing TAM-modulating immunotherapies by targeting the transcriptional factor PU.1.

P=N/A, N=75, Active, not recruiting, Suez Canal University

Luteolin induces ferroptosis by directly targeting GPX4, and promotes antitumor immune responses. These findings reveal a novel mechanism underlying luteolin-induced ferroptosis and provide theoretical support for its immunotherapeutic application in colon cancer.