CX3CR1 (C-X3-C Motif Chemokine Receptor 1)

The review critically evaluates the axis's potential as a biomarker, discusses methodological advances and limitations in human studies, and analyzes therapeutic strategies with a focus on translational challenges. We conclude with a forward-looking perspective on precision medicine approaches targeting this axis.

Strikingly, we find that only constitutive, and not conditional, TCF1 over-expression can increase the size of the stem-like T cell pool. Thus, while TCF1 can slow stem-like T cell differentiation, it is insufficient to revert more differentiated cells back into a stem-like state.

Mechanistically, CI upregulated the expression of ADAM10, which plays a key role in converting membrane-bound CX3CL1 to its soluble form. This study provided evidence that chronic inflammation could promote tumor progression through the activation of ADAM10/CX3CL1 axis in gastric cancer.

Inhibition of MG/Mϕ with long-term minocycline treatment attenuated the incidence of ICHs around bAVMs. Our study indicates that MG/Mϕ are involved in destabilization of KRAS-induced bAVM, leading to hemorrhagic conversion/ICH. Thus, modulation of MG/Mϕ may reduce ICH risk in bAVM patients.

To promote clinical adoption, we propose a roadmap that prioritizes benchmarked workflows (e.g., scverse ecosystem), privacy-aware data sharing via federated learning, and causal AI approaches to disentangle biological signal from technical artifact. By synthesizing computational innovations with translational case studies, this review equips researchers to navigate both the analytical and ethical complexities of scRNA-seq in pursuit of actionable diagnostics.

This study employed multi-parametric flow cytometry and clodronate liposome (CL) depletion to systematically re-evaluate splenic CD11chighMHCIIhigh cDCs in C57BL/6 mice...These findings demonstrate unprecedented cDC plasticity driven by microenvironmental signals, revising conventional classification frameworks and proposing new targets for DC-based immunotherapies in autoimmunity and cancer. Our phenotypic mapping provides a foundational framework for future functional investigations into these novel subsets.

PLAE is associated with sex-specific dysregulation of the CX3CL1/CX3CR1 axis and convergent neuroimmune-vascular signatures indicative of subclinical endothelial dysfunction. These associative findings support the hypothesis that fractalkine-pathway modulation may mitigate long-term neurobehavioral and cardiovascular vulnerability after PLAE, warranting causal testing.

These effects of Cyst-C are abolished by a cell-type-specific deletion (Cx3cr1TREM2-/-) or mutation of TREM2 (TREM2R47H) or Cyst-C (Cyst-CL68Q) in microglia. Together, these findings provide significant conceptual advances into cancer neuroscience and establish therapeutic avenues that are distinct from the present amyloid-lowering strategies, aiming at degrading the existing amyloid plaques for precision-targeted AD therapy.

Targeting CCR5 with genetic knockdown or the approved drug maraviroc impairs GSC stemness and prolongs survival in GBM models. Our work highlights the functional interplay between OLs and GBM cells and positions the CCL5/CCR5 axis as a druggable target in GBM.

RT, either alone or in combined with chemotherapy, significantly alters systemic immunity in HNSCC. Immunophenotyping and peripheral biomarkers show prognostic potential, supporting their integration into personalized treatment strategies. However, standardized, large-scale longitudinal studies are warranted.

We propose that interventions targeting this axis must move beyond traditional agonist/antagonist approaches toward spatiotemporally specific precision control strategies, including intelligent delivery systems, CRISPR-based cell engineering, and AI-driven personalized treatments. Rationally reprogramming the functional orientation of this axis holds promise in overcoming immune checkpoint inhibitor resistance and provides a theoretical foundation for the development of a new generation of cancer immunotherapies.

Macrophages from Il1α⁻/⁻ tumors exhibited activated immune gene signatures similar to human macrophages. These findings reveal that IL-1α drives an immunosuppressive TME partly through PGE2 signaling, highlighting IL-1α as a potential therapeutic target in breast cancer.