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Forced expression of CXCL10 prevents in vitro growth and metastasis of colon carcinoma cells by recruiting natural killer cells.
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upregulated in synovium and chondrocytes following intra-articular fracture
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FNDC4 could suppress osteoclast formation via NF-kappaB pathway and downregulation of CXCL10
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This study explored the effect of CXCL10 on COPD induced by cigarette smoke (CS) and its underlying mechanism.
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CXCL10, not CXCL9 or CXCL11, induced IL-9 expression in the liver tissue.
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in vivo experiments show that the CXCL10/CXC chemokine receptor family 3 axis prevents the recruitment of macrophages, reduces inflammation, and halts the progression of the disease; the increased production of IL-1beta highlights the autoinflammatory nature of congenital hepatic fibrosis and may open novel therapeutic avenues
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CXCL10 and blood-brain barrier permeability enhancement in rabies virus infection
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Study shows that circulating interferon- that binds to receptors on brain endothelial cells and induces Cxcl10, is a central link in the signaling chain eliciting inflammation-induced aversion.
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The knockout of either CXCL10 or TNF-alpha reduced germ cell apoptosis in the co-cultures of germ cells and Sertoli cells in response to MuV infection. Local injection of MuV into the testes of mice confirmed the involvement of CXCL10 in germ cell apoptosis in vivo.
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CXCL10 has strong inhibitory effects on neovascularization, whereas MMP13 is required for neovascularization in C. albicans-infected corneas.
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Study provided the evidence that CXCL10/CXCR3 signaling in periaqueductal gray is involved in the development of morphine analgesic tolerance via neuron-microglia interaction.
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Results suggest that CXCL10(-/-) mice are protected against diet-induced nonalcoholic steatohepatitis (NASH), in an obesity-independent manner.
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In conclusion, upregulated CXCL10 in steatohepatitis impairs autophagic flux by reducing autolysosome formation, thereby inhibiting autophagic protein degradation and the accumulation of ubiquitinated proteins, leading to the development of steatohepatitis.
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These findings highlight the importance of CXCL10 signaling in the pathogenesis of rheumatoid arthritis and provide previously unidentified details of the mechanisms by which CXCL10 promotes the development of arthritis.
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Study revealed that CXCL10 evoked an ionic current mainly carried by Cl(-) channels, suggests that Cl(-) channels are likely key molecular candidates responsible for the CXCL10-evoked neuronal activation and itch-like behaviors in a murine model of allergic contact dermatitis induced by the antigen squaric acid dibutylester. Cl(-) channels may emerge as a promising drug target for the treatment of allergic itch.
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Collectively, these results suggest that the CXCL10/CXCR3-mediated NF-kappaB signaling pathway plays a role in the control of autonomous regulation of CXCL10 and malignant tumor properties in breast cancer 4T1 cells.
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results show an important role for CXCR3 and CXCL10 in the tissue distribution of preimmune memory phenotype CD8 T- cells
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In lipotoxic hepatocytes, MLK3 activates a MAPK signaling cascade, resulting in the activating phosphorylation of STAT1, and CXCL10 transcriptional upregulation.
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These findings elucidate an NFAT-MAPK signaling paradigm for induction of isletokine expression in beta-cells and reveal IP-10 as a primary therapeutic target to prevent beta-cell-induced inflammatory loss of graft function after islet cell transplantation.
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A novel function of CXCL10 in mediating monocyte production of proinflammatory cytokines in inflammatory bowel diseases has been described.
