CXCL16 (C-X-C Motif Chemokine Ligand 16)

Further co-localisation analysis revealed that ADAMTS5, GNLY and PCSK7 shared genetic variants associated with the risk of malignant neoplasms of bone and articular cartilage. Molecular docking analysis indicated that compounds such as aspirin and vitamin E exhibited low binding energies with GNLY, PCSK7 and ADAMTS5, suggesting potential therapeutic intervention opportunities.ConclusionThis study identified three proteins (GNLY, PCSK7 and ADAMTS5) associated with a high risk of malignant neoplasms of bone and articular cartilage through Mendelian randomisation and co-localisation analyses, providing novel molecular evidence for early diagnosis, risk assessment and potential targeted therapies for malignant neoplasms of bone and articular cartilage.

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.

To optimize this strategy, we develop Y101S, an antibody-drug conjugate targeting TGF-β, PD-L1, and STING, which demonstrates superior tumor control and immune modulation in preclinical models. These findings highlight the therapeutic potential of this triple-targeting approach.

CXCL16 promotes macrophage senescence, and senescent CXCL16+ macrophages drive LUAD progression through TGF-β signalling. These findings identify CXCL16+ macrophages as a biologically and therapeutically relevant immune cell population, highlighting a potential target for precision intervention in LUAD.

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.

Functional assays demonstrated that DHA-treated cells exhibited increased secretion of TNF, IL1β, ROS, and PD-L1, accompanied by enhanced cytotoxic activity against hepatocellular carcinoma cells in a co-culture system. These findings reveal the molecular mechanisms underlying TAN polarization, and establish DHA as a potent immunomodulatory agent capable of reshaping TANs toward an anti-tumor phenotype.

Targeting the MDK/LRP1 axis with Resmetirom offers a promising therapeutic strategy for MASH-associated HCC, addressing both metabolic dysfunction and tumor progression.

The major risk factor for ICI myocarditis is the use of combination ICI treatment, especially when relatlimab, a novel anti-LAG-3 (lymphocyte-activation gene 3) antibody, is combined with anti-PD-1 (programmed cell death protein 1) therapy...Treatment with anti-CXCR6 antibody prevented premature lethality, attenuated arrhythmias, and reduced the histological severity of myocarditis, demonstrating that CXCR6+ T cells are necessary for disease pathogenesis. Our findings suggest that ICI myocarditis is driven by an expansion of CXCR6+ T cells and identifies CXCR6 as a putative therapeutic target for this highly morbid condition.

Additionally, METTL5Low human ICC correlates with responsiveness to immunotherapy. The study highlights the strong immuno-evasive ability of METTL5 as a promising therapeutic target in ICC.

In this RNA-Seq analysis, we identified genes that are up- and downregulated in response to acute B. bovis infection. Gene expression of IL-10, along with that of the inflammatory cytokines IL-1β, TNFα and IL-18, suggests a non-protective response to B. bovis at 10 dpi. These results enhance our understanding of the molecular interactions between Babesia and the host immune system.

Structural modeling revealed a compact 3D conformation, a high ratio of hydrophilic to hydrophobic residues, and a unique N-linked glycosylation site. This study provides the first integrated evidence of β-conglycinin's dual role, particularly from lupin, as both a fungal toxin inhibitor and an anticancer agent, highlighting its potential as a safe natural therapeutic.

The infiltration of TNFR2+ Treg cells may reinforce the immunosuppressive milieu of MPE, facilitating disease progression. Collectively, these findings uncover a novel mechanism governing immunosuppression in MPE, providing new insights into potential therapeutic strategies to disrupt this process.