Recombinant human interferon-inducible protein 10 is a chemoattractant for human monocytes and T lymphocytes and promotes T cell adhesion to endothelial cells.

Taub, Dennis D.; Lloyd, Andrew R.; Conlon, Kevin; Wang, Ji Ming; Ortaldo, John R.; Harada, Akihisha; Matsushima, Kouji; Kelvin, David J.; Oppenheim, Joost J.

doi:10.1084/jem.177.6.1809

Cited by 696 publications

(445 citation statements)

References 23 publications

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“…The CXCL10/CXCR3 axis plays a critical role in inflammation by recruiting activated T lymphocytes, monocytes, and macrophages. 12,14,58,60 We found that CXCL10 expression is up-regulated in cells, including RGCs, after axonal injury, which is associated with leukocyte recruitment and infiltration in neural retina. To investigate potential mechanisms of CXCR3-mediated RGC death in TON, we deleted CXCR3 in leukocytes and found that leukocyte recruitment is attenuated and RGC survival is increased.…”

Section: Discussionmentioning

confidence: 78%

Critical Role of the CXCL10/C-X-C Chemokine Receptor 3 Axis in Promoting Leukocyte Recruitment and Neuronal Injury during Traumatic Optic Neuropathy Induced by Optic Nerve Crush

Liu

Zhu

et al. 2017

The American Journal of Pathology

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Traumatic optic neuropathy (TON) is an acute injury of the optic nerve secondary to trauma. Loss of retinal ganglion cells (RGCs) is a key pathological process in TON, yet mechanisms responsible for RGC death remain unclear. In a mouse model of TON, real-time noninvasive imaging revealed a dramatic increase in leukocyte rolling and adhesion in veins near the optic nerve (ON) head at 9 hours after ON injury. Although RGC dysfunction and loss were not detected at 24 hours after injury, massive leukocyte infiltration was observed in the superficial retina. These cells were identified as T cells, microglia/monocytes, and neutrophils but not B cells. CXCL10 is a chemokine that recruits leukocytes after binding to its receptor C-X-C chemokine receptor (CXCR) 3. The levels of CXCL10 and CXCR3 were markedly elevated in TON, and up-regulation of CXCL10 was mediated by STAT1/3. Deleting CXCR3 in leukocytes significantly reduced leukocyte recruitment, and prevented RGC death at 7 days after ON injury. Treatment with CXCR3 antagonist attenuated TON-induced RGC dysfunction and cell loss. In vitro co-culture of primary RGCs with leukocytes resulted in increased RGC apoptosis, which was exaggerated in the presence of CXCL10. These results indicate that leukocyte recruitment in retinal vessels near the ON head is an early event in TON and the CXCL10/CXCR3 axis has a critical role in recruiting leukocytes and inducing RGC death. (Am J Pathol 2017, 187: 352e365; http://dx

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Section: Discussionmentioning

confidence: 78%

Critical Role of the CXCL10/C-X-C Chemokine Receptor 3 Axis in Promoting Leukocyte Recruitment and Neuronal Injury during Traumatic Optic Neuropathy Induced by Optic Nerve Crush

Liu

Zhu

et al. 2017

The American Journal of Pathology

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“…Of all the cytokine genes that are known to be induced in vivo by DMXAA in murine tissues (Cao et al, 2001), only mRNA for IP-10 was up-regulated in cultures of HECPP cells (Figure 2A). IP-10 is known for its chemotactic (Luster et al, 1985;Taub et al, 1993) and anti-angiogenic activities (Angiolillo et al, 1995) but has no reported apoptotic activity. Our results here suggest that DMXAA may have a direct apoptotic effect on endothelial cells.…”

Section: Discussionmentioning

confidence: 99%

Induction of endothelial cell apoptosis by the antivascular agent 5,6-dimethylxanthenone-4-acetic acid

et al. 2002

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5,6-Dimethylxanthenone-4-acetic acid, synthesised in this laboratory, reduces tumour blood flow, both in mice and in patients on Phase I trial. We used TUNEL (TdT-mediated dUTP nick end labelling) assays to investigate whether apoptosis induction was involved in its antivascular effect. 5,6-Dimethylxanthenone-4-acetic acid induced dose-dependent apoptosis in vitro in HECPP murine endothelial cells in the absence of up-regulation of mRNA for tumour necrosis factor. Selective apoptosis of endothelial cells was detected in vivo in sections of Colon 38 tumours in mice within 30 min of administration of 5,6-Dimethylxanthenone-4-acetic acid (25 mg kg −1 ). TUNEL staining intensified with time and after 3 h, necrosis of adjacent tumour tissue was observed. Apoptosis of central vessels in splenic white pulp was also detected in tumour-bearing mice but not in mice without tumours. Apoptosis was not observed in liver tissue. No apoptosis was observed with the inactive analogue 8-methylxanthenone-4-acetic acid. Positive TUNEL staining of tumour vascular endothelium was evident in one patient in a Phase I clinical trial, from a breast tumour biopsy taken 3 and 24 h after infusion of 5,6-Dimethylxanthenone-4-acetic acid (3.1 mg m −2 ). Tumour necrosis and the production of tumour tumour necrosis factor were not observed. No apoptotic staining was seen in tumour biopsies taken from two other patients (doses of 3.7 and 4.9 mg m −2 ). We conclude that 5,6-Dimethylxanthenone-4-acetic acid can induce vascular endothelial cell apoptosis in some murine and human tumours. The action is rapid and appears to be independent of tumour necrosis factor induction. British Journal of Cancer (2002) 86 , 1937–1942. doi: 10.1038/sj.bjc.6600368 www.bjcancer.com © 2002 Cancer Research UK

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“…Binding of ligand to CXCR3 is crucial for chemotaxis of these receptor positive cells to inflammatory sites (5). CXCL10 is regarded as a chemoattractant preferentially for activated T-cells (6) and particularly Th1 cells (7).…”

Section: Macrophages Dendritic Cells and Natural Killer T-cells) Andmentioning

confidence: 99%

Enhanced Expression of CXCL10 in Inflammatory Bowel Disease

Østvik

Granlund

Bugge

et al. 2013

Inflammatory Bowel Diseases

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We explored the gene expression in colonic biopsies of active and inactive inflammatory bowel disease (IBD), in an extensive material of ulcerative colitis (UC) and Crohn`s disease (CD). The chemokine CXCL10 and its receptor CXCR3 were among the upregulated genes.This study examines the expression of CXCL10 and the mechanisms for its release in patients with UC or CD, and in intestinal epithelial cell (IEC) lines. Methods

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Recombinant human interferon-inducible protein 10 is a chemoattractant for human monocytes and T lymphocytes and promotes T cell adhesion to endothelial cells.

Cited by 696 publications

References 23 publications

Critical Role of the CXCL10/C-X-C Chemokine Receptor 3 Axis in Promoting Leukocyte Recruitment and Neuronal Injury during Traumatic Optic Neuropathy Induced by Optic Nerve Crush

Critical Role of the CXCL10/C-X-C Chemokine Receptor 3 Axis in Promoting Leukocyte Recruitment and Neuronal Injury during Traumatic Optic Neuropathy Induced by Optic Nerve Crush

Induction of endothelial cell apoptosis by the antivascular agent 5,6-dimethylxanthenone-4-acetic acid

Enhanced Expression of CXCL10 in Inflammatory Bowel Disease

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