CCR2 (C-C Motif Chemokine Receptor 2)

To address these issues, this study engineered copper-doped ZIF-8 nanoparticles that co-deliver the hypoxia-activated prodrug TH-302 and the NQO1-targeting quinone β-lapachone, encapsulated within genetically engineered M1 macrophage membranes overexpressing CCR2 (CCR2-M)...No drug-related toxicity was observed. Thus, this rationally designed nanotherapeutic strategy significantly curtails residual tumor growth and offers a promising immunomodulatory approach to overcoming therapeutic resistance in cancer treatment after iRFA.

Macrophage depletion abrogates metastasis, while the FABP1 inhibitor orlistat reverses SPP1 upregulation in macrophages...Importantly, virtual screening identifies indole-3-acetic acid (IAA) as an RNF32 inhibitor that suppresses liver metastasis and reverses immunosuppression in vivo. This study establishes RNF32 as a dual-functional driver of metastasis and proposes IAA as a promising therapeutic agent, offering new hope for targeting both tumor-intrinsic EMT and the immune microenvironment in CRC liver metastasis.

The main focus of future studies should be on addressing therapeutic resistance, enhancing combination therapies, and identifying predictive biomarkers to enhance treatment efficacy and patient results. The study reveals complex molecular interactions regulated by CCL2, thus offering a foundation for innovative therapeutic approaches to colorectal cancer.

Acute pharmacologic blockade of TLR5 in tumor-bearing mice altered the composition of tumor-associated myeloid populations, reducing the frequency of monocytes and CCR2-expressing macrophages accumulating within the TME of WT mice. These data reveal that chronic TLR5 signaling, driven by tumor-induced loss of gut barrier integrity, promotes expansion of myeloid cells within the bone marrow and is a host-intrinsic mechanism driving accumulation of immature monocytes and macrophages into the TME.

Given our incomplete understanding of its mechanism, the development of combined strategies or miRNA, epigenetic intervention, and other source regulation methods is necessary. This study provides a theoretical basis for understanding the tumor regulatory network of CCL2 and the development of precise targeted therapy.

Treatment with the Treg-depleting antibody RG6292 suppressed viral transformation in donors that otherwise supported LCL outgrowth, confirming a functional role for Tregs in shaping early EBV infection outcomes. Viral transcript enrichment-seq revealed an upregulation of early lytic and failure to sustain latent gene expression correlating with failure to generate LCL. These findings highlight intact PBMCs as a tractable model to study EBV viral-host interaction in a genetically diverse, human-specific context, and that Tregs play a key determining role in viral transformation.

Compared to MSCs, En-MSCsC/I demonstrated superior migration to injured joints and unique regulatory signature for cartilage regeneration. Our study suggests that En-MSCsC/I may offer enhanced therapeutic effects for RA-related cartilage damage while maintaining favorable safety profiles.

In summary, this study highlights the dual role of CD147 as a potential checkpoint in regulating THP-1 monocyte migration, with its function varying depending on the context and microenvironment. Additionally, CD147KO THP-1 monocytes exhibited a shift in the balance between pro- and anti-inflammatory cytokine responses.

This study is the first to elucidate the crucial involvement of F. nucleatum in shaping cancer-associated adipocytes within the HNSCC microenvironment. F. nucleatum-reprogrammed adipocytes enhance cisplatin resistance via the CCL2-CCR2 axis, offering new therapeutic avenues to overcome chemotherapy resistance in necrotic neck lymph nodes.

The phenotypic characteristics of the CAR-T cells, including memory T cell subsets (stem cell memory and central memory), were analyzed by flow cytometry. Tumor growth inhibition was assessed, and markers of immune exhaustion and evasion were quantified.

Thus, constitutive mTORC1 activation in MΦ depresses pro-inflammatory cell infiltration, increases GPNMB protein expression, and preserves heart function following I/R. This reveals beneficial effects of a MΦ-dependent mTORC1-GPNMB cascade on the post I/R heart.

Mechanistically, GSDME facilitated mitochondrial injury in cardiomyocytes to release mtDNA and activated the STING/NFκB pathway, further targeting the CCL2-CCR2 axis and cardiac inflammation, thereby aggravating DIC. These findings identify GSDME as a potential therapeutic target for DIC.