Correction: The Synergistic Local Immunosuppressive Effects of Neural Stem Cells Expressing Indoleamine 2,3-Dioxygenase (IDO) in an Experimental Autoimmune Encephalomyelitis (EAE) Animal Model

Lee, Young Eun; An, Jaeyeol; Lee, Kee-Hang; Kim, Sung Su; Song, Hye Jin; Pyeon, Hee-Jang; Nam, Hyunwoo; Kang, Kook Hee; Joo, Kyeung Min

doi:10.1371/journal.pone.0148720

Cited by 4 publications

(3 citation statements)

References 1 publication

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“…NSCs normally express low levels of indoleamine 2,3-dioxygenase (IDO), a tryptophan-metabolizing enzyme which has potent immune suppressive activities. In an EAE animal model, systemic injections of NSCs expressing IDO resulted in significant local immune suppression in the cervical lymph nodes and CNS by recruiting regulatory T lymphocytes and reducing the number of activated T lymphocytes during the inflammation in the CNS which induced significantly fewer clinical symptoms and faster recovery [203].…”

Section: Genetically Modified Nscsmentioning

confidence: 99%

Neural Stem Cell-Based Regenerative Approaches for the Treatment of Multiple Sclerosis

et al. 2017

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Multiple sclerosis (MS) is a chronic, autoimmune, inflammatory, and demyelinating disorder of the central nervous system (CNS), which ultimately leads to axonal loss and permanent neurological disability. Current treatments for MS are largely comprised of medications that are either immunomodulatory or immunosuppressive and are aimed at reducing the frequency and intensity of relapses. Neural stem cells (NSCs) in the adult brain can differentiate into oligodendrocytes in a context-specific manner and are shown to be involved in the remyelination in these patients. NSCs may exert their beneficial effects not only through oligodendrocyte replacement but also by providing trophic support and immunomodulation, a phenomenon now known as "therapeutic plasticity." In this review, we first provided an update on the current knowledge regarding MS pathogenesis and the role of immune cells, microglia, and oligodendrocytes in MS disease progression. Next, we reviewed the current progress on research aimed toward stimulating endogenous NSC proliferation and differentiation to oligodendrocytes in vivo and in animal models of demyelination. In addition, we explored the neuroprotective and immunomodulatory effects of transplanted exogenous NSCs on T cell activation, microglial activation, and endogenous remyelination and their effects on the pathological process and prognosis in animal models of MS. Finally, we examined various protocols to generate genetically engineered NSCs as a potential therapy for MS. Overall, this review highlights the studies involving the immunomodulatory, neurotrophic, and regenerative effects of NSCs and novel methods aiming at stimulating the potential of NSCs for the treatment of MS.

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Section: Genetically Modified Nscsmentioning

confidence: 99%

Neural Stem Cell-Based Regenerative Approaches for the Treatment of Multiple Sclerosis

et al. 2017

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“…In addition to ischemic stroke, Alzheimer’s disease is known to often be associated with secondary depression [ 17 , 18 ]. IDO has been reported to increase in disorders, such as Alzheimer’s disease, along with experimental autoimmune encephalomyelitis and multiple sclerosis [ 17 , 19 , 20 ]. These findings support the relationship between depression and IDO.…”

Section: Discussionmentioning

confidence: 99%

Indoleamine 2, 3-dioxygenase is responsible for low stress tolerance after intracerebral hemorrhage

et al. 2023

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In the chronic phase after intracerebral hemorrhage (ICH), the aftereffect-associated lowering of motivation burdens many patients; however, the pathogenic mechanism is unclear. Here, we revealed for the first time that indoleamine 2, 3-dioxygenase (IDO) expression and enzyme activity are increased in the collagenase-induced murine ICH model. IDO is a rate-limiting enzyme situated at the beginning of the kynurenine pathway and converts tryptophan, a source of serotonin (5-hydroxytryptamine; 5-HT), to kynurenine. In this study, we showed that IDO is localized in 5-HTergic neurons. After ICH, the synaptosomal 5-HT level decreased, but this effect was neutralized by subcutaneous injections of 1-methyl tryptophan (MT), a specific IDO inhibitor. These results suggest that ICH-induced IDO weakens the activity of 5-HTergic neurons. Accordingly, we next investigated whether the IDO increase contributes to the depression-like behaviors of ICH mice. The immobility times of tail suspension and forced swimming tests were significantly prolonged after ICH but shortened by the administration of 1-MT. In conclusion, the increased IDO after ICH was found to decrease 5-HT levels and subsequently reduce stress tolerance. These findings indicate that IDO is a novel therapeutic target for the ICH aftereffect-associated lowering of motivation.

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“…With important neurological activity, the KP metabolites exerted neuroprotective or neurotoxic effects by affecting the brain glutamate, cholinergic and dopaminergic neurotransmitter delivery systems ( 90 ). Alterations in the KP had clinical and therapeutic implications, and targeting various KP enzymes was a possible strategy for addressing a variety of immune, cognitive, and neurodegenerative diseases ( 91 , 92 ).…”

Section: Introductionmentioning

confidence: 99%

An Expanded Neuroimmunomodulation Axis: sCD83-Indoleamine 2,3-Dioxygenase—Kynurenine Pathway and Updates of Kynurenine Pathway in Neurologic Diseases

Tan

Guo

2018

Front. Immunol.

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Many neurologic diseases are related to autoimmune dysfunction and a variety of molecules or reaction pathways are involved in the regulation of immune function of the nervous system. Soluble CD83 (sCD83) is the soluble form of CD83, a specific marker of mature dendritic cell, which has recently been shown to have an immunomodulatory effect. Indoleamine 2,3-dioxygenase (IDO; corresponding enzyme intrahepatic, tryptophan 2,3-dioxygenase, TDO), a rate-limiting enzyme of extrahepatic tryptophan kynurenine pathway (KP) participates in the immunoregulation through a variety of mechanisms solely or with the synergy of sCD83, and the imbalances of metabolites of KP were associated with immune dysfunction. With the complement of sCD83 to IDO-KP, a previously known immunomodulatory axis, this review focused on an expanded neuroimmunomodulation axis: sCD83-IDO-KP and its involvement in nervous system diseases.

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Correction: The Synergistic Local Immunosuppressive Effects of Neural Stem Cells Expressing Indoleamine 2,3-Dioxygenase (IDO) in an Experimental Autoimmune Encephalomyelitis (EAE) Animal Model

Cited by 4 publications

References 1 publication

Neural Stem Cell-Based Regenerative Approaches for the Treatment of Multiple Sclerosis

Neural Stem Cell-Based Regenerative Approaches for the Treatment of Multiple Sclerosis

Indoleamine 2, 3-dioxygenase is responsible for low stress tolerance after intracerebral hemorrhage

An Expanded Neuroimmunomodulation Axis: sCD83-Indoleamine 2,3-Dioxygenase—Kynurenine Pathway and Updates of Kynurenine Pathway in Neurologic Diseases

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