CD14 (CD14 Molecule)

Levels of inter-alpha-trypsin inhibitor heavy chain H3 (ITIH3) were significantly elevated in all three screens, with complement C5, complement factors B and H (CFB/CFH), and monocyte differentiation antigen CD14 increased in KPC mice and PDAC patients; and all were significantly increased co-ordinately in PDAC according to disease stage. Serum levels of C5, CFH and CD14 together constitute a novel panel for identifying PanINs and early-stage PDAC with confidence, and when combined with additional screening, could help increase survival from this dismal disease.

Despite the limitations of an in vitro PBMC-based system, selective VEGFR-1 blockade by D16F7 mAb alleviates VEGF-A-driven immune tolerance while preserving T-cell activation, supporting its translational potential as a complementary immunomodulatory approach.

Our findings identify UDP as a potent immunomodulatory metabolite that restricts monocyte proliferation while promoting differentiation into dendritic-like cells with enhanced phagocytic capacity. UDP engages complex transcriptional programs that integrate innate activation with adaptive immune regulation, highlighting its potential role in immune homeostasis and inflammation control.

BA alleviates sepsis-induced liver injury through activating PPARγ and inhibiting CD14/NF-κB pathway, highlighting its potential as a new approach to treatment sepsis.

EVs enriched in platelet (CD49e) and endothelial (CD31) markers were associated with corticosteroid response, whereas EVs enriched with endothelial (CD105 and CD146) and B lymphocyte (CD19) markers were associated with mortality. Overall, EVs enriched in endothelial and monocyte markers may represent a candidate non-invasive tool for predicting corticosteroid response and mortality in AH, aiding risk stratification and early identification of non-responders for timely transplant evaluation.

Functional assays demonstrate that TNF-⍺ enhanced trogocytosis, promoting the formation of CD14+CD4+ T cells. These findings uncover a TNF-⍺-mediated mechanism of immunosuppression in the TME and highlight aberrant myeloid-T cell interactions as contributors to NSCLC progression.

Early-stage HCC induces a reversible, systemic immunosuppressive transcriptome captured by a monocyte-derived 23-gene blood signature; tumor removal partially restores this profile within three months. These results highlight the potential of blood-derived monocyte signatures as noninvasive biomarkers of HCC-associated immunosuppression and clinical outcome.

No single marker provides sufficient accuracy across all healing phases, highlighting the need for multimodal approaches that combine morphological assessment with panels of temporally complementary biomarkers. Standardization of methods and additional high-quality human studies are essential to improve the reliability and forensic applicability of wound age estimation.

0.17]), SAA (β = 0.43, [0.13, 0.17]), sICAM-1 (β = 63.52, [9.92, 117.13]), sVCAM-1 (β = 69.03, [8.29, 129.76]), and TNF-α (β = 0.08, [0.00, 0.16]), and negatively associated with CRP (β = - 0.28, [- 0.49, - 0.08]). Our findings demonstrate a novel pesticide/herbicide-inflammation link in adolescents, which may be an underlying mechanism of the health impacts of pesticides/herbicides.

More importantly, PDC1 demonstrated promising targeting selectivity and improved the tumor-inhibition efficiency in ovarian cancer-xenograft mouse models without systemic toxicity. This multiple protease-activated, disulfide-bridging PDC strategy provides a novel, precise and safe ADC-targeted therapeutics against ovarian cancer.

Our findings underscore the critical role of TLR4 signalling in cachexia-associated muscle wasting across different disease contexts and demonstrate the efficacy of OH-CATH30, a TLR4 inhibitor, in alleviating muscle atrophy in various cachexia models.