Amino Acids Fuel T Cell-Mediated Inflammation

Poffenberger, Maya C.; Jones, Russell G.

doi:10.1016/j.immuni.2014.04.017

Cited by 30 publications

(26 citation statements)

References 10 publications

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“…CD is a Th1-type T cell-mediated inflammation while UC is a Th2-type T cell-mediated inflammation [4]. AAs directly serve as a fuel source for T cells and are considered to have influence on shaping T cell-mediated immune responses [56]. Additionally, the signaling central integrator of environmental stimuli for the regulation of T cell activation and differentiation is mammalian target of rapamycin (mTOR) [57, 58].…”

Section: Amino Acids: Application In Inflammatory Bowel Disease Thmentioning

confidence: 99%

Roles of Dietary Amino Acids and Their Metabolites in Pathogenesis of Inflammatory Bowel Disease

Bao

Feng

Yao³

et al. 2017

Mediators of Inflammation

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Inflammatory Bowel Disease (IBD) is a kind of chronic inflammation, which has increasing incidence and prevalence in recent years. IBD mainly divides into Crohn's disease (CD) and ulcerative colitis (UC). It is hard to cure IBD completely, and novel therapies are urgently needed. Amino acids (AAs) and their metabolites are regarded as important nutrients for humans and animals and also play an important role in IBD amelioration. In the present study, the potential protective effects of AAs and their metabolites on IBD had been summarized with the objective to provide insights into IBD moderating using dietary AAs and their metabolites as a potential adjuvant therapy.

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Section: Amino Acids: Application In Inflammatory Bowel Disease Thmentioning

confidence: 99%

Roles of Dietary Amino Acids and Their Metabolites in Pathogenesis of Inflammatory Bowel Disease

Bao

Feng

Yao³

et al. 2017

Mediators of Inflammation

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“…ASCT2 is a sodium-coupled transporter for neutral amino acids, including glutamine, alanine, serine, threonine and cysteine [100]. A recent report showed that glutamine and glucose uptake are reduced in ASCT2-deficient T cells [97,101]; the latter observation is due to the fact that the glucose receptor, Glut1, is expressed at lower levels in these cells. As a consequence, Asct2 −/− T cells have reduced mTORC1 activation and metabolic defects that specifically attenuate T H 1 and T H 17 differentiation and function [97,101].…”

Section: Mtor Is a Critical Regulator Of T-cell Homeostasis And Functionmentioning

confidence: 99%

“…A recent report showed that glutamine and glucose uptake are reduced in ASCT2-deficient T cells [97,101]; the latter observation is due to the fact that the glucose receptor, Glut1, is expressed at lower levels in these cells. As a consequence, Asct2 −/− T cells have reduced mTORC1 activation and metabolic defects that specifically attenuate T H 1 and T H 17 differentiation and function [97,101]. Further investigation is needed to determine if different amino acids share common transporters to induce functional T-cell responses.…”

Section: Mtor Is a Critical Regulator Of T-cell Homeostasis And Functionmentioning

confidence: 99%

mTOR Signaling, Tregs and Immune Modulation

2014

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Foxp3+ Tregs are central regulators of immune tolerance. As dysregulated Treg responses contribute to disease pathogenesis, novel approaches to target the immunomodulatory functions of Tregs are currently under investigation. mTORC1 and mTORC2 are therapeutic targets of interest. Recent studies revealed that mTOR signaling impacts conventional T-cell homeostasis, activation and differentiation. Moreover, mTOR controls the differentiation and functions of Tregs, suggesting that its activity could be targeted to modulate Treg responses. Here, we summarize how Tregs suppress immune responses, their roles in disease development and methods used to alter their functions therapeutically. We also discuss the diverse effects exerted by mTOR inhibition on the development, homeostasis, and functions of conventional T cells and Tregs. We conclude with a discussion of how modulation of mTOR activity in Tregs may be therapeutically beneficial or detrimental in different disease settings.

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“…Using labeled glucose or glutamine and mass spectrometry analysis to study ATP metabolism, it has been found that less than 20% of glucose in Th1 CD4 + and CD8 + T cells went into the TCA cycle, but that the conversion of glutamine to glutamate, which subsequently entered the TCA cycle, was the major source of ATP (57). Studies using glutamine depletion in vitro showed that reduced glutamine level led to lowered oxidative phosphorylation and ATP production (58). Signaling through the AMP kinase was found to be one mechanism by which T cells respond to changes in nutrient availability (59).…”

Section: Metabolism In Immunotherapymentioning

confidence: 99%

Special Conference on Tumor Immunology and Immunotherapy: A New Chapter

Byrne

Vonderheide

Jaffee

et al. 2015

Cancer Immunology Research

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The overall objective of the fifth American Association for Cancer Research Special Conference on “Tumor Immunology and Immunotherapy: A New Chapter” organized by the Cancer Immunology Working Group was to highlight multidisciplinary approaches of immunotherapy and mechanisms related to the ability of immunotherapy to fight established tumors. With the FDA approval of sipuleucel-T, ipilimumab (anti-CTLA4; Bristol-Myers Squibb [BMS]), and the two anti-PD-1 antibodies, pembrolizumab (formerly MK-3475 or lambrolizumab; Merck) and nivolumab (BMS), immunotherapy has become a mainstream treatment option for some cancer. Many of the data presented at the conference and reviewed in this article showcase the progress made in determining the mechanistic reasons for the success of some treatments and the mechanisms associated with tolerance within the tumor microenvironment, both of which are potential targets for immunotherapy. In addition to combination and multimodal therapies, improvements in existing therapies will be needed to overcome the numerous ways that tumor-specific tolerance thwarts the immune system. This conference built upon the success of the 2012 conference, and focused on seven progressing and/or emerging areas that include: New combination therapies; Combination therapies and vaccine Improvement; Mechanisms of antibody therapy; Factors in the tumor microenvironment affecting the immune response; The microbiomes effect on cancer and immunotherapy; Metabolism in immunotherapy; and Adoptive T-cell therapy.

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Amino Acids Fuel T Cell-Mediated Inflammation

Cited by 30 publications

References 10 publications

Roles of Dietary Amino Acids and Their Metabolites in Pathogenesis of Inflammatory Bowel Disease

Roles of Dietary Amino Acids and Their Metabolites in Pathogenesis of Inflammatory Bowel Disease

mTOR Signaling, Tregs and Immune Modulation

Special Conference on Tumor Immunology and Immunotherapy: A New Chapter

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