Epstein-Barr Virus Infection Induces Indoleamine 2,3-Dioxygenase Expression in Human Monocyte-Derived Macrophages through p38/Mitogen-Activated Protein Kinase and NF-κB Pathways: Impairment in T Cell Functions

Liu, Wanli; Lin, Yongbin; Han, Xiao; Xing, Shan; Chen, Hao; Chi, Peidong; Zhang, Ge

doi:10.1128/jvi.03678-13

Cited by 67 publications

(64 citation statements)

References 41 publications

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“…Furthermore, while TGFβ inhibits IFNγ -induced IDO1 mRNA expression in cultured fibroblasts, TGFβ induces IDO1 expression in pDCs [113,117]. Finally, whereas IL-6 inhibits IDO1 in CD8α + murine DCs, the inflammatory cytokine acts in concert with TNFα to induce IDO1 in virus-infected human monocytederived macrophages [94].…”

Section: Control Of Ido1 Gene Expressionmentioning

confidence: 97%

“…Activation of the NF-κB pathway is important for the induction of IDO1 in response to stimuli other than IFNγ (Figure 2), including LPS [92], GpC-ODNs [107], viral infection [94,108,109] and CD80/CD86 ligation [101]. For example, induction of IDO1 by LPS and virus infection involves the activation of both NF-κB and p38 MAPK (mitogen-activated protein kinase) [92,94].…”

Section: Control Of Ido1 Gene Expressionmentioning

confidence: 98%

“…For example, induction of IDO1 by LPS and virus infection involves the activation of both NF-κB and p38 MAPK (mitogen-activated protein kinase) [92,94]. NF-κB-dependent induction of IRF3-and TGFβ (transforming growth factor β)-dependent induction of IDO1 in response to TLR9-activation by GpC-ODNs involves novel roles for TRIF [TIR (Toll/interleukin-1 receptor) domaincontaining adaptor protein inducing interferon β] and TRAF6 (TNF-receptor-associated factor 6) proteins [107].…”

Section: Control Of Ido1 Gene Expressionmentioning

confidence: 99%

“…The binding of TNFα to its receptor stimulates the NF-κB (nuclear factor κB) pathway, enhancing IRF1 transcription and STAT1 activation to up-regulate the expression of IFNγ receptors, thereby potentiating IFNγ signalling [66,[74][75][76][77]. Other stimuli that can induce IDO1 expression in various cell types, either singly or in combination with IFNγ , include type I IFNs (IFNα and IFNβ), IFNλ, IL (interleukin)-1 and IL-6, TLR (Toll-like receptor) 3, 4, 7, 8 and 9 ligands, thymosin α 1 , oestrogen, PGE 2 (prostaglandin E 2 ), muramyl tripeptide, α-galactosylceramide, glucocorticoids and haemoglobin [74,75,[78][79][80][81][82][83][84][85][86][87][88][89][90][91][92][93][94][95][96] and certain infectious pathogens (discussed in detail in the 'IDO1 and host response to microbial infection' section below).…”

Section: Control Of Ido1 Gene Expressionmentioning

confidence: 99%

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Role of indoleamine 2,3-dioxygenase in health and disease

et al. 2015

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IDO1 (indoleamine 2,3-dioxygenase 1) is a member of a unique class of mammalian haem dioxygenases that catalyse the oxidative catabolism of the least-abundant essential amino acid, L-Trp (L-tryptophan), along the kynurenine pathway. Significant increases in knowledge have been recently gained with respect to understanding the fundamental biochemistry of IDO1 including its catalytic reaction mechanism, the scope of enzyme reactions it catalyses, the biochemical mechanisms controlling IDO1 expression and enzyme activity, and the discovery of enzyme inhibitors. Major advances in understanding the roles of IDO1 in physiology and disease have also been realised. IDO1 is recognised as a prominent immune regulatory enzyme capable of modulating immune cell activation status and phenotype via several molecular mechanisms including enzyme-dependent deprivation of L-Trp and its conversion into the aryl hydrocarbon receptor ligand kynurenine and other bioactive kynurenine pathway metabolites, or non-enzymatic cell signalling actions involving tyrosine phosphorylation of IDO1. Through these different modes of biochemical signalling, IDO1 regulates certain physiological functions (e.g. pregnancy) and modulates the pathogenesis and severity of diverse conditions including chronic inflammation, infectious disease, allergic and autoimmune disorders, transplantation, neuropathology and cancer. In the present review, we detail the current understanding of IDO1's catalytic actions and the biochemical mechanisms regulating IDO1 expression and activity. We also discuss the biological functions of IDO1 with a focus on the enzyme's immune-modulatory function, its medical implications in diverse pathological settings and its utility as a therapeutic target.

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Section: Control Of Ido1 Gene Expressionmentioning

confidence: 97%

Section: Control Of Ido1 Gene Expressionmentioning

confidence: 98%

Section: Control Of Ido1 Gene Expressionmentioning

confidence: 99%

Section: Control Of Ido1 Gene Expressionmentioning

confidence: 99%

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Role of indoleamine 2,3-dioxygenase in health and disease

et al. 2015

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“…Liao et al (27) used NPC cell lines to detect that IL-6 promoted NPC cell proliferation in a dose-and time-dependent manner, and this was accompanied by increasing cyclin D1 and Bcl-2 expression, STAT-3 activation, and inhibition of Bax and p21 expression. Liu et al (28) observed that in certain macrophages of the tumor stroma of NPC tissue, IL-6-and TNF-α-dependent expression of tryptophan-catabolizing enzyme indoleamine 2,3-dioxygenase led to suppressed proliferation of T cells and impaired cytotoxic activity of CD8(+) T cells, thus facilitating immune escape.…”

Section: Discussionmentioning

confidence: 99%

Pre-treatment serum inflammatory cytokines as survival predictors of patients with nasopharyngeal carcinoma receiving chemoradiotherapy

Al-Kholy

Abdullah

Abadier

et al. 2016

Molecular and Clinical Oncology

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Abstract. The present study aimed to examine the predictability of pre-treatment serum levels of interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α for determining the outcome of patients with nasopharyngeal carcinoma (NPC) assigned for chemoradiotherapy. A total of 35 patients with NPC were subjected to clinical examination and evaluation of performance status using Karnofsky scoring. Nasopharyngoscopy was performed for evaluation and to obtain a biopsy. Blood samples were obtained pre-and post-treatment for polymerase chain reaction quantitative estimation of Epstein-Barr virus (EBV) DNA plasma load and enzyme-linked immunosorbent assay for estimation of serum cytokines. All patients received chemoradiotherapy and were followed-up for 2 years. Cervical lymphadenopathy and recurrent attacks of epistaxis are the most common presenting symptoms. Treatment significantly decreased pre-treatment plasma EBV DNA load and serum levels of IL-6 and TNF-α, and increased serum IL-1β levels. Clinical staging and EBV DNA plasma load revealed positively significant correlation with pre-treatment serum levels of both IL-6 and TNF-α, while revealed negative significant correlation with serum IL-1β levels. The 2-year survival rate was negatively significantly correlated with pre-treatment levels of IL-6 and TNF-α, and EBV DNA viral load, while it was positively significantly correlated with pre-treatment performance scores and serum IL-1β levels. Statistical analyses defined high pre-treatment serum IL-6 levels as a significant specific predictor for high mortality rate. It was demonstrated that NPC was associated with high pre-treatment plasma EBV DNA load and serum cytokines, and chemoradiotherapy significantly reduced these high levels. High pre-treatment serum IL-6 level was a significant specific predictor for high mortality rate. Increased post-treatment serum levels of IL-1β indicated good therapeutic response and most probably a high survival rate.

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N‐(3′,4′‐dimethoxycinnamonyl) anthranilic acid alleviates severe acute pancreatitis by inhibiting intestinal barrier dysfunction and NF‐κB activation

Zhao

Lü

2020

Drug Development Research

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Severe acute pancreatitis (SAP) can affect intestinal barrier with a high mortality. To date, effective therapies for SAP are still in urgently need. The purpose of this study was to investigate the role of anthranilic acid active synthetic derivative, N‐(3′,4′‐dimethoxycinnamonyl) anthranilic acid (3,4‐DAA), in intestinal barrier dysfunction of SAP. In this study, SAP mice model was induced by caerulein combined with lipopolysaccharide (LPS). SAP mice were pretreated with 3,4‐DAA orally. Histological structures of pancreatic and intestinal tissues were observed via hematoxylin–eosin (H&E) staining. Pancreas myeloperoxidase (MPO), serum lipase, and amylase were detected using corresponding kits. Western blot analysis and reverse transcription and quantitative PCR (RT‐qPCR) were employed to determine the levels of inflammatory factors in both pancreatic and intestinal tissues. Moreover, the levels of intestinal barrier‐related proteins, NLRP3 inflammasome and NF‐κB pathway were examined by western blot analysis. Result revealed that 3,4‐DAA significantly attenuated pancreas and intestine damage, inhibited the release of inflammatory factors and intestinal barrier dysfunction. Moreover, the expression of NLRP3 and phospho‐NF‐κB p65 in pancreatic and intestinal tissues was notably suppressed by 3,4‐DAA. To sum up, these results demonstrated that 3,4‐DAA could ameliorate SAP, partly attributing to the inhibition of intestinal barrier dysfunction and the release of inflammatory factors. These findings may provide a new mechanism support for 3,4‐DAA application in the clinical treatment of SAP.

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Epstein-Barr Virus Infection Induces Indoleamine 2,3-Dioxygenase Expression in Human Monocyte-Derived Macrophages through p38/Mitogen-Activated Protein Kinase and NF-κB Pathways: Impairment in T Cell Functions

Abstract: Epstein-Barr virus (EBV) infection has been observed in tumor-infiltrated macrophages, but its infection effects on macrophage

Cited by 67 publications

References 41 publications

Role of indoleamine 2,3-dioxygenase in health and disease

Role of indoleamine 2,3-dioxygenase in health and disease

Pre-treatment serum inflammatory cytokines as survival predictors of patients with nasopharyngeal carcinoma receiving chemoradiotherapy

N‐(3′,4′‐dimethoxycinnamonyl) anthranilic acid alleviates severe acute pancreatitis by inhibiting intestinal barrier dysfunction and NF‐κB activation

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