MRC1 (Mannose Receptor C-Type 1)

Our findings unveil CCL11 as a master regulator of the pro-tumorigenic niche post-resection, driving recurrence through coordinated immune evasion and promoting tumor invasiveness. Targeting the CCL11-CCR5/CCR3 axis presents a promising strategy to improve HCC surgical outcomes.

In the SCCVII model, aging impaired the antitumor immune responses, associated with early recruitment of M2-like TAMs. PD-1 expression in aged TME CD8T was impaired, but the PD-L1 blockade increased PD-1 expression, suggesting that the site of action for PD-L1 blockade differs between young and aged mice.

Complement activation and the accumulation of M2-like macrophages are associated with anti-human MDA5 monoclonal antibody-induced hepatic injury in mice. These findings provide mechanistic insight into antibody-complement-macrophage interactions and suggest that modulation of complement pathways may represent a potential therapeutic approach to limit liver and systemic involvement in this disorder.

It was also linked to reduced cisplatin/paclitaxel sensitivity (P < 0.05) and lower immunotherapy response (29.04% vs. 45.05%, P = 0.015). These findings suggest that JAML deficiency may suppress cyclic GMP-AMP synthase (cGAS)-STING pathway activation, potentially contributing to M1/M2 macrophage polarization imbalance and facilitating EC progression. Clinically, JAML expression shows promise as a potential biomarker for prognostic stratification and treatment response prediction (chemotherapy/immunotherapy), providing insights for developing precision immunochemotherapy strategies in EC.

In a mouse model of HCC, neoadjuvant PD-1 immune checkpoint inhibition can modulate the immunosuppressive tumor microenvironment observed after cryoablation. This highlights the potential of a combination therapy to treat both early- and advanced-stage HCC.

These findings suggest that dysregulated gene expression may contribute to the activation of stromal cells and macrophages within the spleen, facilitating malignant transformation. Overall, these findings deliver novel transcriptomic insights into canine splenic tumorigenesis that may improve diagnostic precision, inform prognostic assessment, and support the development of targeted therapeutic strategies in veterinary oncology.

In vivo, AQP4-IgG-induced EVs-mtDNA exacerbated microglial activation and NMO through the TLR9/MyD88/NF-κB pathway. AQP4-IgG-induced EVs carried mtDNA to upregulate TLR9, further activating the MyD88/NF-κB pathway, thereby promoting microglial activation and transition toward pro-inflammatory gene-high-expressing cells to drive NMO progression.

In addition, suppressing or overexpressing METTL3, YTHDF1, and NMDAR2B correspondingly decreased or increased these effects, but modulation of NMDAR2B did not change the expression of METTL3/YTHDF1. rTMS can affect the polarization state of microglia and neuroinflammation by regulating the METTL3/NMDAR2B/NLRP3 signaling pathway, thereby improving NeuP.

STE reprograms TAMs via the JAK1/STAT1 axis and exhibits robust antitumor activity, underscoring its promise as a natural, macrophage-targeted immunotherapeutic that warrants further investigation for integration into cancer treatment strategies.

Preclinical studies demonstrate CSF-1R inhibitors (e.g., pexidartinib) disrupt LSC-TAM crosstalk, while CAR-M therapy synergizes with phagocytosis-promoting agents. Despite challenges, macrophage-targeted therapies offer transformative potential by remodeling the TME, overcoming resistance, and augmenting immunotherapy. This review outlines mechanistic insights and translational strategies to harness macrophage plasticity for leukemia treatment.

Importantly, CFI did not affect TC cell-autonomous proliferation, suggesting that its pro-tumoural effects are mediated by the TME rather than directly on tumour cells. Collectively, Our findings establish RARγ/CFI signalling as a microenvironmental rheostat controlling TAM polarisation and provide new insights into the immunobiology of thyroid cancers.

Genetically modified sFgl2-MSCs alleviate renal I/R injury. This protective effect is associated with engagement of neutrophil CD32b receptors, activation of the TGFβ-Smad2/3 pathway, promotion of a protective N2-like neutrophil phenotype, and suppression of N1-like and NET-related markers.