CCR2 (C-C Motif Chemokine Receptor 2)

Forty-eight successfully modeled rats were randomly divided into a model group, an acupuncture group, a fluoxetine group, and an acupuncture+agonist group, with 12 rats in each group...Compared with the acupuncture+agonist group, the acupuncture group showed better improvement in all indexes (P<0.05). Tongdu Tiaoshen acupuncture could improve neurological function and depressive-like behavior in PSD rats, possibly by inhibiting the CCL2-CCR2 pathway and promoting neuronal synaptic remodeling in the hippocampus.

Furthermore, immunohistochemical analysis revealed increased CCL2 protein expression in the affected spinal cords. These findings suggest that systemic immune activation contributes to spinal neuroinflammation in DM, although its limited cellular infiltration implies a minor role in neurodegeneration.

Translational entry points include selective HIF-2α inhibition, phosphoinositide 3-kinase gamma (PI3Kγ) blockade, SUCNR1 targeting, and exosome-based miRNA modulation, while a biomarker panel comprising HIF-1α, vascular endothelial growth factor A (VEGF-A), and MMP-9 offers a pragmatic readout of hypoxia burden, macrophage programming, and therapeutic response. We conducted a focused narrative review (PubMed, Scopus, Web of Science; English; 2003-2025), prioritizing mechanistic and translational studies on hypoxia-HIF, lactate/succinate, and hypoxia-regulated exosomes across T2D, atherosclerosis, and cancer.

64Cu-DOTA-ECL1i PET accurately detected the expression of CCR2 in patients with HNSCC. The effectiveness of propagermanium in the inhibition of MOC1 tumor progression indicated its potential for HNSCC therapy.

Emerging therapeutic strategies aim to disrupt this axis by depleting Tregs (e.g., anti-CD25), blocking MDSC recruitment (e.g., CCR2 inhibitors), or reprogramming TAMs (e.g., CD40 agonists), often in combination with programmed death 1/programmed death-ligand 1 blockade. An integrated approach targeting these populations holds promise for converting pancreatic ductal adenocarcinoma into an immunologically responsive tumor.

This humanized model replicates ICI-AIN key features, revealing a synergistic role of ICIs and pro-inflammatory cytokines. TNF-α blockade demonstrated protective effects, supporting its potential role in mitigating the risk of ICI-AIN.

It eliminates both non-MYCN-amplified (SH-SY5Y and SK-N-SH) and MYCN-amplified (SMS-KCNR) NB cells that exhibit PMA-inducible CCL2 expression but not MYCN-amplified NB cells (IMR-32 and NB-1) that exhibit CCL2 repression, and is offset by reciprocal NB cell-induced Fas-mediated Jurkat cell apoptosis. These findings form a solid foundation for further pre-clinical development aimed at identifying clinically relevant physiological immune cell equivalents and alternative PKC activators, with the ultimate goal of translating this mechanism into an effective immune-therapeutic approach for the treatment of high-risk non-immunogenic NBs, especially NBs that exhibit CCL2 and TrkAIII expression.

It describes their impact on bone destruction, bone marrow angiogenesis, chemoresistance, and the recruitment of cells into the MM niche, such as macrophages, myeloid-derived suppressor cells, and cytotoxic lymphocytes, along with their effects on mesenchymal stromal cells. A bioinformatic analysis highlights the significance of these chemokines in MM, and the possibility of targeting them in MM therapy is also considered.

Distinct CD45+ immune landscapes, characterized by inflammatory suppression in LLC1 and metabolic adaptation in KrasLA2 tumors, shape lung tumor biology. This atlas identifies genotype-specific immune vulnerabilities with potential relevance for precision immunotherapy in non-small cell lung cancer.

ZIKV-driven activation and recruitment of CCR2+ monocytes supports robust anti-tumor CD8+ T cell responses by enhancing cytotoxicity and limiting exhaustion. These findings highlight the previously unappreciated therapeutic potential of modulating monocyte-T cell crosstalk to overcome immune suppression in GBM.

Our study identifies fibroblast-immune cell interactions, particularly IL-6-mediated fibroblast-macrophage crosstalk, as a key mechanism in radioimmunotherapy-induced cardiac fibrosis. Tocilizumab, an IL-6R inhibitor, demonstrates therapeutic potential to attenuate this cardiotoxicity.

Comprehensive single-cell analysis identified selective chemokine recruitment signatures supporting γδ T-cell infiltration but revealed paradoxical corecruitment of immunosuppressive populations. Patient stratification through chemokine profiling, combined with γδ T-cell enrichment and targeted chemokine antagonism, represents a rational therapeutic strategy.