CXCL10 expression

CEP alleviates NASH by inhibiting lipogenesis and inflammatory responses in a STAT1/CXCL10 axis-dependent manner.

Combined high expression of TLR6 and CXCL10 correlated with a better prognosis in ESCC patients. This suggests that PGN reduces cell proliferation and tumor progression through a PGN-TLR-CXCL10 cascade, thereby influencing prognosis after esophagectomy for ESCC, and that improving the oral environment could potentially improve the prognosis of ESCC patients after esophagectomy.

Tomatidine can alleviate neuronal damage in SCI by inhibiting apoptosis and inflammation through the NF-κB/CXCL10 pathway. Our findings provide a novel therapeutic target and candidate for the treatment of SCI.

We identify IFNϵ loss as the elusive 9p21 link to human immune-cold, CXCL9/10-CXCR3 axis-depleted tumors. Extending mouse-model studies of IFN-I on TME immune-cell levels, we found that IFNϵ loss is the primary cell-intrinsic 9p21 immune signal to DC and macrophage subtype and subcluster expression of CXCL9 and CXCL10, the major sources of these chemokines. Larger deletions to 9p24 further restrict CXCL9/10 induction via loss of IFN-γ-pathway gene, JAK2. 9p-loss tumors with these distinct IFN defects operative in the TME, lack the capacity of endogenous CXCL9/10 induction in an immune-desert, ICT-resistant state. These data, the extensive 9p loss/ICT resistance body of evidence, and early NSCLC DC-chemokine vaccine trials, have led to a DC vaccine engineered with a CXCL9/10 payload, designed to bypass the specific, severe chemokine deficit in 9p loss tumors.

The inhibition of ROS using N-acetylcysteine (NAC) eliminated the apoptosis effects of LYD, resulting in increased cell viability...Furthermore, LYD also exerts its antitumor effects by inhibiting crucial proteins involved in cell growth. Overall, LYD shows promise as a potential therapeutic agent for NSCLC treatment.

We also investigate how the IRF2-CXCL10 pathway induces T cell exhaustion and leads to immune escape. This research provides new insights into the immunotherapy of bladder cancer, highlighting potential molecular targets for more effective treatment strategies.

We revealed that the HIF1A inhibitors echinomycin (EC) and YC-1 upregulated CXCL10/11 genes induced by IFN-γ in tumor cells in vitro...Combination therapy enhanced tumor infiltration of CD8 T cells and suppressed tumor angiogenesis. The present study suggests that HIF1A signaling in tumor cells dominates ICI resistance via the downregulation of tumor-derived CXCL10/11.

We identified key regulators of pTLS density in patients with HCC and proposed a non-invasive radiomic classifier capable of assisting in stratification for prognosis and treatment.

Enhancing IFN-I cytokine production and blocking PGE2 secretion restores this process and re-sensitizes tumours to T cell-mediated immunity. Together, our work uncovers a central role of inflammatory monocytes in intratumoral T cell stimulation, elucidates how oncogenic signalling disrupts T cell responses through counter-regulation of PGE2 and IFN-I, and proposes rational combination therapies to enhance immunotherapies.

P1, N=28, Completed, Jennie Taylor | Active, not recruiting --> Completed

CXCL10 expression can be predicted noninvasively and preoperatively via radiomic signatures based on contrast-enhanced CT images.

Hmox1highiCAFs overexpressed the Cxcl10 receptor (Sdc4) and facilitated functional CD8+ T-cell infiltration through the Tnfsf9-Tnfrsf9 axis. Overall, our nanodrugs reshape the phenotype of CAFs and enhance functional CD8+ T-cell infiltration into tumors, holding the potential to be a safe and promising therapy for PDAC.