Vitamin C Promotes Maturation of T-Cells

Manning, Jared; Mitchell, Birgitta; Appadurai, Daniel A.; Shakya, Arvind; Pierce, Laura Jean; Wang, Hongfang; Nganga, Vincent; Swanson, Patrick C.; May, James M.; Tantin, Dean; Spangrude, Gerald J.

doi:10.1089/ars.2012.4988

Cited by 135 publications

(135 citation statements)

References 41 publications

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“…Sepsis significantly weakened the proliferation and IFN- γ secretion but enhanced the apoptotic level and IL-4 secretion of CD4 + CD25 − T cells of WT mice and Gulo −/− mice; however, treatment with 200 mg/Kg parenteral Vit C for two times after CLP significantly took a turn for the better and acted on upregulating the proliferative response and IFN- γ secretion as well as downregulating the apoptotic rate and IL-4 secretion. The immunological mechanisms of Vit C on CD4 + T cells have not been elucidated; reactive oxygen species (ROS) was formed during CD4 + T cells activation which acted as the second messenger [19–21, 27]. We conjectured that parenteral Vit C affects T cell behaviors during sepsis via ROS.…”

Section: Discussionmentioning

confidence: 99%

The Parenteral Vitamin C Improves Sepsis and Sepsis-Induced Multiple Organ Dysfunction Syndrome via Preventing Cellular Immunosuppression

Gao

Lü

Zhai

et al. 2017

Mediators of Inflammation

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Cellular immunosuppression appears to be involved in sepsis and sepsis-induced multiple organ dysfunction syndrome (MODS). Recent evidence showed that parenteral vitamin C (Vit C) had the ability to attenuate sepsis and sepsis-induced MODS. Herein, we investigated the impact of parenteral Vit C on cellular immunosuppression and the therapeutic value in sepsis. Using cecal ligation and puncture (CLP), sepsis was induced in WT and Gulo−/− mice followed with 200 mg/Kg parenteral Vit C administration. The immunologic functions of CD4+CD25+ regulatory T cells (Tregs) and CD4+CD25− T cells, as well as the organ functions, were determined. Administration of parenteral Vit C per se markedly improved the outcome of sepsis and sepsis-induced MODS of WT and Gulo−/− mice. The negative immunoregulation of Tregs was inhibited, mainly including inhibiting the expression of forkhead helix transcription factor- (Foxp-) 3, cytotoxic T lymphocyte associated antigen- (CTLA-) 4, membrane associated transforming growth factor-β (TGF-βm+), and the secretion of inhibitory cytokines [including TGF-β and interleukin- (IL-) 10], as well as CD4+ T cells-mediated cellular immunosuppression which was improved by parenteral Vit C in WT and Gulo−/− septic mice. These results suggested that parenteral Vit C has the ability to improve the outcome of sepsis and sepsis-induced MODS and is associated with improvement in cellular immunosuppression.

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Section: Discussionmentioning

confidence: 99%

The Parenteral Vitamin C Improves Sepsis and Sepsis-Induced Multiple Organ Dysfunction Syndrome via Preventing Cellular Immunosuppression

Gao

Lü

Zhai

et al. 2017

Mediators of Inflammation

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“…Cultures were initiated in 12 well plates in complete media (Schmitt and Zuniga-Pflucker, 2002) supplemented with 10ng/ml Flt-3 and 10ng/ml IL-7 (Biosource) and 30nM L-ascorbic acid (1-ascorbic acid-2-phosphate sesquimagnesium salt; SIGMA) (Manning et al, 2013). YS and FL from E10.5 embryos were seeded at 2 embryos equivalent per well.…”

Section: Methodsmentioning

confidence: 99%

Distinct Genetic Networks Orchestrate the Emergence of Specific Waves of Fetal and Adult B-1 and B-2 Development

et al. 2016

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SUMMARY B cell development is often depicted as a linear process initiating in the fetus and continuing postnatally. Using a PU.1 hypomorphic mouse model, we found that B-1 and B-2 lymphopoiesis occurred in distinct fetal and adult waves differentially dependent on the Sfpi1 14 kB upstream regulatory element. The initial wave of fetal B-1 development was absent in PU.1 hypomorphic mice, while subsequent fetal and adult waves emerged. In contrast, B-2 lymphopoiesis occurred in distinct fetal and adult waves. Whole transcriptome profiling of fetal and adult B cell progenitors supported the existence of three waves of B-1 and two waves of B-2 development, and revealed that the network of transcription factors governing B lineage specification and commitment was highly divergent between B-1 and B-2 progenitors. These findings support the view that the B-1 and B-2 lineages are distinct and provide a genetic basis for layering of immune system development.

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“…For example, ascorbate enhances T cell maturation, an effect that is intrinsic to lymphoid cells and independent of T cell receptor (TCR) rearrangement. Inhibition of DNA and histone methylation further promotes the effect of ascorbate on T-cell differentiation, which suggests a role of ascorbate participated active demethylation of DNA and histone in T cell maturation (55). …”

Section: Vitamin C and Histone Demethylationmentioning

confidence: 99%

Regulation of the Epigenome by Vitamin C

Young¹,

2015

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Emerging evidence suggests that ascorbate, the dominant form of vitamin C under physiological pH conditions, influences the genome activity via regulating epigenomic processes. Ascorbate serves as a cofactor for ten-eleven translocation (TET) dioxygenases that catalyze the oxidation of 5-methylcytosine (5mC) into 5-hydroxymethylcytosine (5hmC), further to 5-formylcytosine (5fC) and 5-carboxylcytosine (5caC), which are ultimately replaced by unmodified cytosine. The JmjC domain-containing histone demethylases also require ascorbate as a cofactor for histone demethylation. Thus, by primarily participating in the demethylation of both DNA and histones, ascorbate appears to be a mediator of the interface between the genome and environment. Furthermore, redox status has a profound impact on the bioavailability of ascorbate in the nucleus. In order to bridge the gap between redox biology and genomics, we suggest an interdisciplinary research field that can be termed “Redox Genomics” to study dynamic redox processes in health and diseases. This review examines the evidence and potential molecular mechanism of ascorbate in demethylation of the genome, while highlighting potential epigenetic roles of ascorbate in various diseases.

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Vitamin C Promotes Maturation of T-Cells

Cited by 135 publications

References 41 publications

The Parenteral Vitamin C Improves Sepsis and Sepsis-Induced Multiple Organ Dysfunction Syndrome via Preventing Cellular Immunosuppression

The Parenteral Vitamin C Improves Sepsis and Sepsis-Induced Multiple Organ Dysfunction Syndrome via Preventing Cellular Immunosuppression

Distinct Genetic Networks Orchestrate the Emergence of Specific Waves of Fetal and Adult B-1 and B-2 Development

Regulation of the Epigenome by Vitamin C

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