2002
DOI: 10.1016/s0041-1345(02)03560-1
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Study of the effect of indoleamine 2,3-dioxygenase on murine mixed lymphocyte reactions and skin allograft rejection

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Cited by 13 publications
(11 citation statements)
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“…T cell activation is sensitive to local tryptophan concentrations, and lack of tryptophan blocks their proliferation [40] . By degrading tryptophan, IDO inhibits T cell proliferation and plays a role in autoimmunity and anti-inflammatory responses [41][42][43] . For example, Apoe -/-mice treated with the IDO inhibitor, 1-methyl-Trp, showed a significant increase in atherosclerotic lesions in the aortic arch and root of their hearts along with enhanced vascular inflammation [41] .…”
Section: Microenvironmentmentioning
confidence: 99%
“…T cell activation is sensitive to local tryptophan concentrations, and lack of tryptophan blocks their proliferation [40] . By degrading tryptophan, IDO inhibits T cell proliferation and plays a role in autoimmunity and anti-inflammatory responses [41][42][43] . For example, Apoe -/-mice treated with the IDO inhibitor, 1-methyl-Trp, showed a significant increase in atherosclerotic lesions in the aortic arch and root of their hearts along with enhanced vascular inflammation [41] .…”
Section: Microenvironmentmentioning
confidence: 99%
“…The immunomodulatory function of IDO was first identified in the placenta, where it inhibits the rejection of fetal allografts (2,4). Subsequent studies documented that IDO inhibits T cell proliferation in vitro (4,5), promotes the survival of allografts (6)(7)(8), and ameliorates both experimental autoimmune encephalomyelitis (9) and trinitrobenzenesulfonic acid-induced colitis (10).…”
Section: Inhibition Of Nf-b and Induction Of Apoptosis Is Specific Tomentioning
confidence: 99%
“…While it is tempting to speculate that Trp catabolism serves as an endogenous counter-regulatory mechanism to limit inflammation, evidence of its role in autoimmune diseases is limited. For instance, inhibition of IDO activity in an animal model of MS results in exacerbated disease [64,65]. Conversely, genetic ablation of IDO in mice does not result in overt, immediate autoimmune disease [41], indicating that the absence of IDO-mediated Trp catabolism per se is not sufficient to unleash autoimmunity.…”
Section: Trp Degradation As a Therapeutic Mechanism In Autoimmune Infmentioning
confidence: 99%