Induction of endotoxin tolerance inhibits alloimmune responses

Ishiyama, K.; Ohdan, Hideki; Tokita, Daisuke; Shishida, Masayuki; Tanaka, Yuka; Irei, Toshimitsu; Asahara, Toshimasa

doi:10.1016/j.trim.2006.06.002

Cited by 13 publications

(18 citation statements)

References 26 publications

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“…DCs in particular appear to be immature and their activation appears to be impaired as evidenced by reduced production of chemokine (C-C motif) ligand 3 (CCL3) and CCL5 (Albrecht et al 2008), reduced levels of CD80 and CD86 (Cohen et al 2004) and evidence of reduced numbers (Ishiyama et al 2006). …”

Section: State Of Leukocytes In Endotoxin Tolerancementioning

confidence: 99%

“…Curiously, while there is evidence of reduced numbers of DCs as a whole (Ishiyama et al 2006), it would appear that the relative proportion of myeloid DCs increases leading to a higher level of antigenic stimulation overall, in turn leading to the differentiation of naïve T cells along the Th2 pathway but producing T lymphocytes with a characteristically reduced expression of IL-2 and interferon gamma (IFNγ) but normal levels of IL-4 and IL-5 (Ishiyama et al 2006; Lauw et al 2000). …”

Section: State Of Leukocytes In Endotoxin Tolerancementioning

confidence: 99%

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Myalgic encephalomyelitis or chronic fatigue syndrome: how could the illness develop?

et al. 2019

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A model of the development and progression of chronic fatigue syndrome (myalgic encephalomyelitis), the aetiology of which is currently unknown, is put forward, starting with a consideration of the post-infection role of damage-associated molecular patterns and the development of chronic inflammatory, oxidative and nitrosative stress in genetically predisposed individuals. The consequences are detailed, including the role of increased intestinal permeability and the translocation of commensal antigens into the circulation, and the development of dysautonomia, neuroinflammation, and neurocognitive and neuroimaging abnormalities. Increasing levels of such stress and the switch to immune and metabolic downregulation are detailed next in relation to the advent of hypernitrosylation, impaired mitochondrial performance, immune suppression, cellular hibernation, endotoxin tolerance and sirtuin 1 activation. The role of chronic stress and the development of endotoxin tolerance via indoleamine 2,3-dioxygenase upregulation and the characteristics of neutrophils, monocytes, macrophages and T cells, including regulatory T cells, in endotoxin tolerance are detailed next. Finally, it is shown how the immune and metabolic abnormalities of chronic fatigue syndrome can be explained by endotoxin tolerance, thus completing the model.

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Section: State Of Leukocytes In Endotoxin Tolerancementioning

confidence: 99%

Section: State Of Leukocytes In Endotoxin Tolerancementioning

confidence: 99%

Myalgic encephalomyelitis or chronic fatigue syndrome: how could the illness develop?

et al. 2019

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“…These results imply the diversity of effects of LPS isolated from different bacterial sources on DC-mediated immune functions. LPS is a product of Gram-negative bacteria that leads to tolerance in vivo [43,44], but the molecular mechanisms of LPS-induced tolerance remain obscure. It has been shown that LPS treatment of DCs results in activation of Th2 cells and Tregs and inhibition of inflammatory responses in EAE [13,45,46]; however, it is not known whether or not LPStreated DCs can affect the activity of Th17 cells, which are necessary for EAE induction.…”

Section: B220mentioning

confidence: 99%

Immunotherapy using lipopolysaccharide-stimulated bone marrow-derived dendritic cells to treat experimental autoimmune encephalomyelitis

Zhou

Ćirić

Zhang

et al. 2014

Clinical and Experimental Immunology

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SummaryLipopolysaccharide (LPS) produced by Gram-negative bacteria induces tolerance and suppresses inflammatory responses in vivo; however, the mechanisms are poorly understood. In this study we show that LPS induces apoptosis of bone marrow-derived dendritic cells (DCs) and modulates phenotypes of DCs. LPS treatment up-regulates expression of toleranceassociated molecules such as CD205 and galectin-1, but down-regulates expression of Gr-1 and B220 encephalomyelitis (EAE) development and down-regulates expression of retinoic acid-related orphan receptor gamma t (ROR-γt), interleukin (IL)-17A, IL-17F, IL-21, IL-22 and interferon (IFN)-γ in myelin oligodendrocyte glycoprotein (MOG)-primed CD4 + T cells in the peripheral environment. These results suggest that LPS-induced apoptotic DCs may lead to generation of tolerogenic DCs and suppress the activity of MOGstimulated effector CD4+ T cells, thus inhibiting the development of EAE in vivo. Our results imply a potential mechanism of LPS-induced tolerance mediated by DCs and the possible use of LPS-induced apoptotic DCs to treat autoimmune diseases such as multiple sclerosis.

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“…Impaired antigen presentation is also seen in DCs following IDO activation and the phenomenon is driven by the same mechanism discussed in the context of macrophages above (550). In this state, DC activation of naïve T cells leads to Th-2 polarisation (551,552). The activity of these DCs may inhibit the activity of memory and effector T cells, encourage the development of CD4 and CD8 T cell anergy, and induce production and the activation of Tregs (553,554).…”

Section: Chronic Nitro-oxidative Stress and The Advent Of Immunosuppressionmentioning

confidence: 90%

Redox Regulation of the Immune Response: Nitro-Oxidative Stress and Antioxidants Regulate Macrophage, Neutrophil, and T and B Lymphocyte, and Dendritic and Natural Killer Cell Functions

Morris¹,

Maes²

2021

Preprint

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An immune-inflammatory response is accompanied by increased nitro-oxidative stress. The aims of this mechanistic review are to review: a) the role of redox sensitive transcription factors and enzymes, ROS/RNS production and the activity of cellular antioxidants on the activation and performance of macrophages, dendritic cells, neutrophils, T cells, B cells and natural killer cells; b) the involvement of high-density lipoprotein (HDL), apolipoprotein (Apo)A1, paraoxonase (PON)-1, and oxidized phospholipids in the regulation of the immune response; and c) the detrimental effects of hypernitrosylation and chronic nitro-oxidative stress on the immune response. The redox changes during immune-inflammatory responses are orchestrated by the actions of nuclear factor (NF)-κB, HIF1alpha, the mechanistic target of rapamycin (mTor), the phosphatidylinositol 3‑kinase (PI3K) / protein kinase B (AKT) signalling pathway, mitogen-activated protein (MAP) kinases, 5' AMP-activated protein kinase (AMPK), and peroxisome proliferator-activated receptor (PPAR). The performance and survival of individual immune cells is under redox control and sensitive to intracellular and extracellular levels of ROS/RNS and is heavily influenced by cellular anti-oxidants including the glutathione and thioredoxin systems, nuclear factor erythroid 2-related factor 2 (Nrf-2), and the HDL complex. Chronic nitro-oxidative stress and hypernitrosylation inhibit the activity of those antioxidant systems, the tricarboxylic acid cycle, mitochondrial functions, and the metabolism of immune cells. In conclusion, those redox-associated mechanisms modulate metabolic reprogramming of immune cells, macrophage and T helper cell polarization, phagocytosis, production of pro- versus anti-inflammatory cytokines, immune training and tolerance, chemotaxis, pathogen sensing, antiviral and antibacterial effects, Toll-like receptor activity, and endotoxin tolerance.

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Induction of endotoxin tolerance inhibits alloimmune responses

Cited by 13 publications

References 26 publications

Myalgic encephalomyelitis or chronic fatigue syndrome: how could the illness develop?

Myalgic encephalomyelitis or chronic fatigue syndrome: how could the illness develop?

Immunotherapy using lipopolysaccharide-stimulated bone marrow-derived dendritic cells to treat experimental autoimmune encephalomyelitis

Redox Regulation of the Immune Response: Nitro-Oxidative Stress and Antioxidants Regulate Macrophage, Neutrophil, and T and B Lymphocyte, and Dendritic and Natural Killer Cell Functions

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