Nitric Oxide Mediates Apoptosis Through Formation of Peroxynitrite and Fas/Fas-Ligand Interactions in Experimental Autoimmune Uveitis

Liversidge, Janet; Dick, Andrew D.; Gordon, Sharon

doi:10.1016/s0002-9440(10)64913-9

Cited by 84 publications

(61 citation statements)

References 55 publications

(54 reference statements)

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“…The CD11b + monocytes found in the heart are not typical MDSCs; phenotypically, the CD11b + heart-infiltrating cells represent a heterogeneous population of largely immature F4/80, CD14, CD45 and CXCR4-positive monocytes, expressing low levels of MHC class II and Gr-1 (51). These findings are consistent with an early study by Liversidge et al (54) that used a mouse model of autoimmune uveoretinitis. The study showed the accumulation of NO-producing monocytes in the choroid and retina of the eye, which was correlated with the severity of disease.…”

Section: Mdscs and Experimental Autoimmune Myocarditis (Eam)supporting

confidence: 92%

Myeloid-derived suppressor cells and myeloid regulatory cells in cancer and autoimmune disorders

Barnie

Zhang

et al. 2016

Experimental and Therapeutic Medicine

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Abstract. Myeloid-derived suppressor cells (MDSCs) were originally described as a heterogeneous population of immature cells derived from myeloid progenitors with immune-suppressive functions in tumor-bearing hosts. In recent years, increasing number of studies have described various populations of myeloid cells with MDSC-like properties in murine models of cancer and autoimmune diseases. These studies have observed that the populations of MDSCs are increased during inflammation and autoimmune conditions. In addition, MDSCs can effectively suppress T cell responses and modulate the activity of natural killer cells and other myeloid cells. MDSCs have also been implicated in the induction of regulatory T cell production. Furthermore, these cells have the potential to suppress the autoimmune response, thereby limiting tissue injury. Myeloid regulatory cells (Mregs) are recently attracting increasing attention, since they function in proinflammatory and immune suppression in autoimmune diseases, as well as in various types of cancer. Currently, research focus is directed from MDSCs to Mregs in cancer and autoimmune diseases. The present study reviewed the suppressive roles of MDSCs in various autoimmune murine models, the immune modulation of MDSCs to T helper 17 lymphocytes, as well as the proinflammatory and immunosuppressive roles of Mregs in various types of cancer and autoimmune diseases.

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Section: Mdscs and Experimental Autoimmune Myocarditis (Eam)supporting

confidence: 92%

Myeloid-derived suppressor cells and myeloid regulatory cells in cancer and autoimmune disorders

Barnie

Zhang

et al. 2016

Experimental and Therapeutic Medicine

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“…Peroxynitrite has been implicated in several other animal models of retinal diseases including experimental autoimmune uveitis in which staining for nitrotyrosine, lipid peroxidation, and apoptosis occurs in photoreceptor cells [41,42], diabetic retinopathy [43], and ischemiareperfusion [44]. The relatively high levels of NO in the retina may be a liability in any disease in which oxidative stress plays a role.…”

Section: Discussionmentioning

confidence: 99%

Blockade of neuronal nitric oxide synthase reduces cone cell death in a model of retinitis pigmentosa

Komeima

Usui

Shen

et al. 2008

Free Radical Biology and Medicine

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Retinitis pigmentosa (RP) is a group of diseases in which many different mutations cause rod photoreceptor cells to die and then gradually cone photoreceptors die due to progressive oxidative damage. In this study, we have shown that peroxynitrite-induced nitrosative damage also occurs. In the rd1 mouse model of RP, there was increased staining for S-nitrosocysteine and nitrotyrosine protein adducts that are generated by peroxynitrite. Peroxynitrite is generated from nitric oxide (NO) and superoxide radicals. After degeneration of rods, injection of hydroethidine resulted in strong fluorescence in the retina of rd1 mice indicating high levels of superoxide radicals, and this was reduced, as was nitrotyrosine staining, by apocynin suggesting that over action of NADP(H) oxidase is at least partially responsible. Treatment of rd1 mice with a mixture of nitric oxide synthase (NOS) inhibitors markedly reduced S-nitrosocysteine and nitrotyrosine staining and significantly increased cone survival, indicating that NO-derived peroxynitrite contributes to cone cell death. Treatment with 7-nitroindazole, a relatively specific inhibitor of neuronal NOS, also significantly reduced cone cell death, but aminoguanidine, a relatively specific inhibitor of inducible NOS, did not. These data suggest that NO generated by neuronal NOS exacerbates oxidative damage to cones in RP and that combined therapy to reduce NO and oxidative stress should be considered.

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“…The presence of 3Ј-nitrotyrosine and 3Ј-nitrotyrosine-modified proteins (protein-associated nitrotyrosine (NYP)) has been reported in a wide spectrum of diseases with an inflammatory component including atherosclerosis (5,6), respiratory disease (7), transplant rejection (8), multiple sclerosis (9), Alzheimer's disease (10), Parkinson's disease (11), celiac disease (12), arthritis (13,14), ischemia-reperfusion injury (15), autoimmune diabetes (16), autoimmune uveitis (17) as well as various cancer and infectious disease settings (18). Despite the fact that the formation of NYP is widely recognized as a surrogate marker of inflammatory processes, the immunological consequence of NYP accumulation has received surprisingly little attention.…”

mentioning

confidence: 99%

Conversion of Tyrosine to the Inflammation-Associated Analog 3′-Nitrotyrosine at Either TCR- or MHC-Contact Positions Can Profoundly Affect Recognition of the MHC Class I-Restricted Epitope of Lymphocytic Choriomeningitis Virus Glycoprotein 33 by CD8 T Cells

Hardy

Wick

Webb

2008

The Journal of Immunology

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Immunohistochemical detection of increased levels of protein-associated nitrotyrosine has become widely used as a surrogate marker of in situ inflammation. However, the potential consequences of protein-associated nitrotyrosine formation in terms of cellular immune recognition has received surprisingly little attention. Using a well-defined I-EK-restricted epitope of pigeon cytochrome c, we previously demonstrated that conversion of a single tyrosine residue to nitrotyrosine can have a profound effect on recognition by CD4 T cells. In this study, we used the MHC class I-restricted epitope of lymphocytic choriomeningitis virus glycoprotein (gp33) to demonstrate that conversion of tyrosine to nitrotyrosine can also profoundly affect recognition of MHC class I-restricted epitopes. Conversion of the Y4 residue of the gp33 epitope to nitrotyrosine completely abrogated recognition by gp33-specific T cells from P14 TCR-transgenic mice. In contrast, CD8+ T cells specific for “nitrated gp33” (NY-gp33) can be readily elicited in C57BL/6 mice after immunization with NY-gp33 peptide. Interestingly, T-T hybridomas specific for NY-gp33 peptide were found to fall into two distinct subsets, being specific for NY-gp33 presented in the context of either H-2Db or H-2Kb. This latter result is surprising in light of previous structural studies showing that Y4 comprises a critical TCR-contact residue when presented by H-2Db but that the same residue points downward into the peptide-binding groove of the MHC when presented by H-2Kb. Together, these results indicate that nitrotyrosine formation can impact T cell recognition both directly, through alteration of TCR-contact residues, or indirectly, through alterations in MHC-contact positions.

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Nitric Oxide Mediates Apoptosis Through Formation of Peroxynitrite and Fas/Fas-Ligand Interactions in Experimental Autoimmune Uveitis

Cited by 84 publications

References 55 publications

Myeloid-derived suppressor cells and myeloid regulatory cells in cancer and autoimmune disorders

Myeloid-derived suppressor cells and myeloid regulatory cells in cancer and autoimmune disorders

Blockade of neuronal nitric oxide synthase reduces cone cell death in a model of retinitis pigmentosa

Conversion of Tyrosine to the Inflammation-Associated Analog 3′-Nitrotyrosine at Either TCR- or MHC-Contact Positions Can Profoundly Affect Recognition of the MHC Class I-Restricted Epitope of Lymphocytic Choriomeningitis Virus Glycoprotein 33 by CD8 T Cells

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