CXCL10/IP-10 in infectious diseases pathogenesis and potential therapeutic implications

Liu, Mingli; Guo, Shanchun; Hibbert, Jacqueline M.; Jain, Vidhan; Singh, Neeru; Wilson, Nana O.; Stiles, Jonathan K.

doi:10.1016/j.cytogfr.2011.06.001

Cited by 514 publications

(556 citation statements)

References 130 publications

(206 reference statements)

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“…Chemokines direct leukocyte trafficking and positioning within tissues (23). In some autoimmune disorders, CXCL10 levels in the affected tissues correlated with local infiltration of T lymphocytes, suggesting that CXCR3/CXCL10 signaling plays an important role in the recruitment of T cells into the site of inflammation and autoimmune attack (39). Indeed, CXCR3/CXCL10 signaling has been impli- + cells values in prostate tissue from nontransferred NOD-SCID mice.…”

Section: Discussionmentioning

confidence: 99%

Expression of CXCR3 on Specific T Cells Is Essential for Homing to the Prostate Gland in an Experimental Model of Chronic Prostatitis/Chronic Pelvic Pain Syndrome

Breser

Motrich

Sánchez

et al. 2013

The Journal of Immunology

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Experimental autoimmune prostatitis (EAP) is considered a valid model for the human disease chronic prostatitis/chronic pelvic pain syndrome. In this report, we analyzed phenotypic characteristics of T cells that gain access to the prostate and induce leukocyte recruitment in mice with different susceptibility to EAP. After EAP induction, NOD mice developed a specific cellular response characterized by a mixed Th1/Th17 pattern with specific T cells mainly expressing CXCR3 that infiltrated and damaged the prostate. In contrast, BALB/c mice, as well as NOD-IFN-γ−/−, exhibited only Th17 cells mainly expressing CCR6 that were not capable of infiltrating the prostate gland. Adoptive transfer experiments of T cells from NOD or NOD–IFN-γ−/− mice to NOD-SCID recipients showed that only T cells from NOD mice successfully infiltrated the prostate. However, after “in vitro” or “in vivo” treatment with rIFN-γ, T cells from NOD–IFN-γ−/− mice became capable of homing to the prostate and induced leukocyte recruitment. Chemokine levels in prostate tissue from NOD mice showed increased expression levels of CXCR3 ligands. Additional experiments using adoptive transfer of sorted CXCR3+CD3+ T cells or administrating a CXCR3 antagonist treatment confirmed these previous results. Altogether, our results demonstrate that the expression of CXCR3 on effector T cells is essential for their homing to the prostate gland in EAP. CXCR3 emerges as a potential therapeutic target to control chronic prostatitis/chronic pelvic pain syndrome.

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Section: Discussionmentioning

confidence: 99%

Expression of CXCR3 on Specific T Cells Is Essential for Homing to the Prostate Gland in an Experimental Model of Chronic Prostatitis/Chronic Pelvic Pain Syndrome

Breser

Motrich

Sánchez

et al. 2013

The Journal of Immunology

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“…Elevated IP-10 levels have been associated with pathogenesis of numerous diseases (Liu et al, 2011). IP-10 levels were significantly elevated in fatal as compared with non-fatal, nonhaemorrhagic YFV human infections (ter Meulen et al, 2004), YFV-17D-infected IFN-a/b/c receptor knockout mice (Thibodeaux et al, 2012), in DENV-infected mice and humans (Fink et al, 2007;Rathakrishnan et al, 2012;Sung et al, 2012), in the spleen and brain tissues of WNVinfected mice (Shirato et al, 2004), and correlated with liver damage in hepatitis C virus-infected patients (Liu et al, 2011). It has been proposed that IP-10 could promote haemorrhagic fever by affecting vascular permeability (Liu et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

Spectrum of disease outcomes in mice infected with YFV-17D

Erickson

Pfeiffer

2015

Journal of General Virology

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“…CCL2 signaling through CCR2 is a key factor in the recruitment and activation of monocytes/macrophages, as well as in the recruitment of T cells to mucosal lesions (24)(25)(26). CXCL10 is a ligand for the CXCR3 receptor, the activation of which results in the recruitment of T cells and the perpetuation of mucosal inflammation (27).…”

Section: Introductionmentioning

confidence: 99%

Tacrolimus (FK506) suppresses TNF-α-induced CCL2 (MCP-1) and CXCL10 (IP-10) expression via the inhibition of p38 MAP kinase activation in human colonic myofibroblasts

Aomatsu

Imaeda

Takahashi

et al. 2012

International Journal of Molecular Medicine

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Abstract. In order to investigate the molecular mechanisms underlying the immunosuppressive effects of tacrolimus (FK506) on intestinal inflammation, we examined whether FK506 effects cytokine/chemokine secretion in human colonic myofibroblasts. Human colonic myofibroblasts were isolated from normal human colonic tissue. The mRNA and protein expression for human CCL2 and CXCL10 were analyzed by real-time PCR and ELISA, respectively. p38 MAP kinase activation was evaluated by western blotting. Tacrolimus (1 µM) suppressed tumor necrosis factor (TNF)-α-induced CCL2 and CXCL10 mRNA expression, but did not modulate TNF-α-induced interleukin (IL)-6 or CXCL8 mRNA expression. Dose-dependent, inhibitory effects of tacrolimus on CCL2 and CXCL10 expression were observed at the mRNA and protein levels. Significant inhibitory effects of tacrolimus were observed at concentrations as low as 0.5 µM for CCL2 and 0.1 µM for CXCL10, respectively. TNF-α-induced CCL2 and CXCL10 expression depended on p38 MAP kinase activation, and tacrolimus strongly inhibited the TNF-α-induced phosphorylation of p38 MAP kinase. Tacrolimus did not affect interferon (IFN)-γ-induced signaling transducer and activator of transcription (STAT)-1 phosphorylation, nor did it modulate CXCL10 mRNA and protein expression. In conclusion, tacrolimus suppressed CCL2 and CXCL10 expression in human colonic myofibroblasts. These inhibitory effects of tacrolimus may play key roles in the therapeutic effects of colonic inflammation in inflammatory bowel disease (IBD) patients.

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CXCL10/IP-10 in infectious diseases pathogenesis and potential therapeutic implications

Cited by 514 publications

References 130 publications

Expression of CXCR3 on Specific T Cells Is Essential for Homing to the Prostate Gland in an Experimental Model of Chronic Prostatitis/Chronic Pelvic Pain Syndrome

Expression of CXCR3 on Specific T Cells Is Essential for Homing to the Prostate Gland in an Experimental Model of Chronic Prostatitis/Chronic Pelvic Pain Syndrome

Spectrum of disease outcomes in mice infected with YFV-17D

Tacrolimus (FK506) suppresses TNF-α-induced CCL2 (MCP-1) and CXCL10 (IP-10) expression via the inhibition of p38 MAP kinase activation in human colonic myofibroblasts

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