Induction of pulmonary indoleamine 2,3-dioxygenase by intraperitoneal injection of bacterial lipopolysaccharide.

Yoshida, Ryotaro; Hayaishi, Osamu

doi:10.1073/pnas.75.8.3998

Cited by 160 publications

(95 citation statements)

References 17 publications

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“…IDO is expressed in nearly every cell type, excluding hepatic cells, and is particularly highly expressed in the lungs and placenta (218). Infection by Chlamydia (26) or Streptococcus (172), as well as stimulation with IFN-␥ (238) or LPS (237), induces IDO expression and results in decreased tryptophan levels. This is an important defensive mechanism, as it creates an innate nutritional barrier that limits the ability of microbes to replicate.…”

Section: Nutritional Defensesmentioning

confidence: 99%

Subversion of Host Recognition and Defense Systems by Francisella spp

Jones

Napier

Sampson

et al. 2012

Microbiol Mol Biol Rev

125

151

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SUMMARY Francisella tularensis is a Gram-negative intracellular pathogen and the causative agent of the disease tularemia. Inhalation of as few as 10 bacteria is sufficient to cause severe disease, making F. tularensis one of the most highly virulent bacterial pathogens. The initial stage of infection is characterized by the “silent” replication of bacteria in the absence of a significant inflammatory response. Francisella achieves this difficult task using several strategies: (i) strong integrity of the bacterial surface to resist host killing mechanisms and the release of inflammatory bacterial components (pathogen-associated molecular patterns [PAMPs]), (ii) modification of PAMPs to prevent activation of inflammatory pathways, and (iii) active modulation of the host response by escaping the phagosome and directly suppressing inflammatory pathways. We review the specific mechanisms by which Francisella achieves these goals to subvert host defenses and promote pathogenesis, highlighting as-yet-unanswered questions and important areas for future study.

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Section: Nutritional Defensesmentioning

confidence: 99%

Subversion of Host Recognition and Defense Systems by Francisella spp

Jones

Napier

Sampson

et al. 2012

Microbiol Mol Biol Rev

125

151

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“…44,45 Moreover, the activity of IDO on the induction of a specific inhibitory environment during chronic infection has recently been revisited. In particular, IFN-dependent expression of IDO by different cell subsets, including DCs, is often seen during infections and represents an innate mechanism of pathogen elimination.…”

Section: Infectionsmentioning

confidence: 99%

The role of indoleamine 2,3-dioxygenase in the induction of immune tolerance: focus on hematology

Curti

Trabanelli

Salvestrini

et al. 2009

Blood

230

195

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The regulation of the interaction between the immune system and antigens, which may lead to the induction of immune tolerance, is critical both under physiologic conditions and in different pathological settings. In the past few years, major strides have been made in our understanding of the molecular and cellular bases of this process. Novel IntroductionIndoleamine 2,3-dioxygenase (IDO) is an intracellular hemecontaining enzyme that catalyzes the initial rate-limiting step in tryptophan degradation along the kynurenine pathway. 1 Tryptophan starvation by IDO consumption inhibits T-cell activation, 1-3 whereas products of tryptophan catabolism, such as kynurenine derivatives and O 2 free radicals, regulate T-cell proliferation and survival. 1,4 IDO is widely expressed in human tissues and cell subsets and is induced during inflammation by IFN-␥ and other inflammatory cytokines. 5 Recent works have demonstrated a crucial role for IDO in the induction of immune tolerance during infection, pregnancy, transplantation, autoimmunity, and neoplasias, including hematologic malignancies. 1,6,7 In the hematology field, regulatory dendritic cells (DCs) and bone marrow (BM)-derived mesenchymal stem cells (MSCs) expressing IDO have the capacity to suppress T-cell responses to autoantigens and alloantigens. 8,9 Moreover, acute myeloid leukemia (AML) cells have been recently demonstrated to express a functionally active form of the IDO protein, which is capable of inhibiting the T-cell response through the expansion of regulatory T cells (T regs ). 10 Although several reviews addressing the enzymatic activity of IDO have recently been published, the aim of the present paper is to summarize the most recent data about IDO expression in hematopoietic cells and its role as a potential therapeutic target in hematologic malignancies. General and biologic aspectsTryptophan is an amino acid required by all life forms for protein synthesis and other important metabolic functions, such as the synthesis of the essential cellular factor, nicotinamide adenine dinucleotide (NADϩ) and the synthesis of serotonin. Dietary tryptophan is delivered to the liver through the hepatic portal system, and the pool of tryptophan that is not used for protein synthesis can either be degraded in the liver or distributed into the bloodstream where it is captured and used by cells throughout the body. Since the 1970s, several studies have demonstrated that 2 different enzymes initiate the catabolism of tryptophan through a series of metabolic steps known collectively as the kynurenine pathway. Tryptophan 2,3-dioxygenase, or TDO, is an enzyme that is primarily expressed in the liver, is induced by tryptophan and metabolic steroids, and is highly specific for tryptophan. In contrast, IDO is found in many tissues, is induced by inflammatory stimuli, and has less substrate specificity. More recently, a novel gene with homology to IDO has been reported and then subsequently demonstrated to encode an enzyme that catabolizes tryptophan. 11,12 This enzyme has bee...

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“…IDO can be induced in vitro or in vivo by various agents like cytokines (IFN-␥, TNF-␣), CD40L, CTLA4-Ig, influenza virus, or bacterial LPS (32)(33)(34)(35)(36)(37). Several subsets of IDO-expressing DC have been described.…”

Section: -Methyl-tryptophan Can Interfere With Tlr Signaling Inmentioning

confidence: 99%

1-Methyl-Tryptophan Can Interfere with TLR Signaling in Dendritic Cells Independently of IDO Activity

Agaugué

Perrin-Cocon

Coutant

et al. 2006

The Journal of Immunology

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The compound 1-methyl-tryptophan (1-MT) is a competitive inhibitor of IDO that can break tolerance and induce fetus, graft, and tumor rejection. Because of its broad effect on immune-related mechanisms, the direct action of 1-MT on human monocyte-derived dendritic cells (DC) was analyzed. It is shown here that the effect of 1-MT on DC is dependent on the maturation pathway. Although 1-MT had no effect on DC stimulated by the TLR3 ligand poly(I:C), it strongly enhanced the Th1 profile of DC stimulated with TLR2/1 or TLR2/6 ligands. Drastic changes in the function of DC stimulated by the TLR4 ligand LPS were induced by 1-MT. These cells could still activate allogeneic and syngeneic T cells but stimulation yielded T cells secreting IL-5 and IL-13 rather than IFN-γ. This action of 1-MT correlated with an increased phosphorylation of p38 and ERK MAPKs and sustained activation of the transcription factor c-Fos. Inhibiting p38 and ERK phosphorylation with synthetic inhibitors blocked the effect of 1-MT on LPS-stimulated DC. Thus, 1-MT can modulate DC function depending on the maturation signal and independently of its action on IDO. This is consistent with previous observations and will help further understanding the mechanisms of DC polarization.

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Induction of pulmonary indoleamine 2,3-dioxygenase by intraperitoneal injection of bacterial lipopolysaccharide.

Cited by 160 publications

References 17 publications

Subversion of Host Recognition and Defense Systems by Francisella spp

Subversion of Host Recognition and Defense Systems by Francisella spp

The role of indoleamine 2,3-dioxygenase in the induction of immune tolerance: focus on hematology

1-Methyl-Tryptophan Can Interfere with TLR Signaling in Dendritic Cells Independently of IDO Activity

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