Regulation and Development
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Initially, the proinflammatory cytokine IL-6 and subsequent Stat3 signaling were found to dictate the fate of these two subsets. Nowadays, more sophisticated mechanisms underlying T-cell fate decisions are being identified: these include cytokines, cellular metabolic pathways, dietary nutrients and the microbiota.
The metabolic mediator mammalian target of rapamycin mTOR is closely involved in this transition. Interestingly though, mTORC1 signaling is necessary for proper Treg cell proliferation and function because deletion of Treg cell-specific Raptor, a component of mTORC1, abrogates the suppressive function of Treg cells and eventually leads to inflammatory disorders. However, enhanced mTOR signaling also reduces the immunosuppressive function of Treg cells. In parallel with this, uncontrolled Akt signaling in Treg cells due to Treg-specific PTEN deficiency results in increased glycolysis and loss of Foxp3.
It is also interesting to note that the same group reported that CK2 is necessary for proper Treg cell function during suppression of type 2 immune responses in the lung; this contradicts another study that examined the effect of CK2 on Treg cells. In Th17 cells, but not Treg cells, glycolysis is linked with de novo fatty acid synthesis by acetyl-CoA carboxylase; this is because Treg cells acquire fatty acids from the environment. Disruption of acetyl-CoA carboxylase results in blockade of Th17 cell differentiation and instead promotes Treg cell differentiation.
Understanding the mechanism s underlying Treg cell development is a prerequisite for Treg cell-based immunotherapy. Using Treg cells for immunotherapy would enable target-specific immunosuppression; this has clear benefits over nonspecific drug-induced immunosuppression, which can induce side effects such as opportunistic infection and cancer induction.
Also, memory Treg cells could provide long-term, hopefully lifelong, tolerance to target antigens, resulting in relatively fewer treatments. Treg cell-mediated immunotherapy could be applied to organ transplantation, autoimmune diseases and allergies, resulting in improved prognoses and fewer side effects. There are more than 60 clinical trials currently registered in the United States examining the utility of Treg cell transfer or indirect methods of boosting Treg cells e.
Most of those trials rely on polyclonal Treg cells derived from donors, although such cells are not target-specific.
In Regulation and Development Jean-Jacques Laffont provides the first theo- retical analysis of regulation of public services for developing countries. He. By Jean-Jacques Laffont; Abstract: In Regulation and Development Jean- Jacques Laffont provides the first theoretical analysis of regulation of public.
To improve specificity, some trials have utilized donor-alloantigen-reactive Treg cells, which are recipient Treg cells that are activated by, and proliferate in, donor tissue. The most recent attempt involves application of a chimeric antigen receptor technique to target Treg cells to specific antigens or more broad alloantigens. Treg cell research has progressed at an astonishing pace over the past two decades. Appreciation of the mechanisms underlying Treg cell development has led to the first therapeutic applications involving Treg cell induction.
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Yet, the fundamental question of how Treg cells enter fates different from Tconv cells even though they arise from a common progenitor T cell still remains unclear. Future studies of the processes underlying development of Treg cells should focus on comprehensive analyses of the entire TCR repertoire, intra- and intercellular mechanisms that determine Treg cell fate, and distinct features between thymic and peripheral Treg cell development. Nishizuka Y, Sakakura T. Thymus and reproduction: sex-linked dysgenesia of the gonad after neonatal thymectomy in mice.
Science ; : — Study on cellular events in postthymectomy autoimmune oophoritis in mice. Requirement of Lyt-1 effector cells for oocytes damage after adoptive transfer. J Exp Med ; : — Gershon RK, Kondo K. Cell interactions in the induction of tolerance: the role of thymic lymphocytes. Immunology ; 18 : — A new I subregion I-J marked by a locus Ia-4 controlling surface determinants on suppressor T lymphocytes. Immunologic self-tolerance maintained by activated T cells expressing IL-2 receptor alpha-chains CD Breakdown of a single mechanism of self-tolerance causes various autoimmune diseases.
J Immunol ; : — Control of regulatory T cell development by the transcription factor Foxp3. Nat Immunol ; 4 : — Nat Genet ; 27 : 20— Shevach EM. The resurrection of T cell-mediated suppression. Blood ; : — Nature ; : — Epigenetic control of the foxp3 locus in regulatory T cells.
PLoS Biol ; 5 : e Cancer Res ; 69 : — Guidance of regulatory T cell development by Satb1-dependent super-enhancer establishment. Nat Immunol ; 18 : — Immunity ; 31 : — Nuclear factor-kappaB modulates regulatory T cell development by directly regulating expression of Foxp3 transcription factor. Transcription factors Foxo3a and Foxo1 couple the E3 ligase Cbl-b to the induction of Foxp3 expression in induced regulatory T cells.
Nat Immunol ; 11 : — Nat Immunol ; 9 : — Function of a Foxp3 cis -element in protecting regulatory T cell identity. Cell ; : — Positive and negative transcriptional regulation of the Foxp3 gene is mediated by access and binding of the Smad3 protein to enhancer I. Immunity ; 33 : — Control of the inheritance of regulatory T cell identity by a cis element in the Foxp3 locus.
Nr4a receptors are essential for thymic regulatory T cell development and immune homeostasis. Nat Immunol ; 14 : — Genes Dev ; 14 : — Methylation matters: binding of Ets-1 to the demethylated Foxp3 gene contributes to the stabilization of Foxp3 expression in regulatory T cells.
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J Mol Med Berl ; 88 : — The Ets-1 transcription factor controls the development and function of natural regulatory T cells. Ascorbate induces ten-eleven translocation Tet methylcytosine dioxygenase-mediated generation of 5-hydroxymethylcytosine.
J Biol Chem ; : — Ascorbic acid enhances Tet-mediated 5-methylcytosine oxidation and promotes DNA demethylation in mammals. J Am Chem Soc ; : — Vitamin C facilitates demethylation of the Foxp3 enhancer in a Tet-dependent manner. Control of Foxp3 stability through modulation of TET activity. Development and maintenance of regulatory T cells.
Immunity ; 38 : — T cell receptor stimulation-induced epigenetic changes and Foxp3 expression are independent and complementary events required for Treg cell development. Immunity ; 37 : — A mechanism for expansion of regulatory T-cell repertoire and its role in self-tolerance.
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Metabolites produced by commensal bacteria promote peripheral regulatory T-cell generation. Commensal microbe-derived butyrate induces the differentiation of colonic regulatory T cells. Int Immunol ; 18 : — Foxp3 transcription-factor-dependent and -independent regulation of the regulatory T cell transcriptional signature.
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Immunity ; 27 : — Regulatory T-cell functions are subverted and converted owing to attenuated Foxp3 expression. Foxp3-dependent programme of regulatory T-cell differentiation. A two-step process for thymic regulatory T cell development. Immunity ; 28 : — T cell receptor signal strength in Treg and iNKT cell development demonstrated by a novel fluorescent reporter mouse. Morikawa H, Sakaguchi S. Genetic and epigenetic basis of Treg cell development and function: from a FoxP3-centered view to an epigenome-defined view of natural Treg cells.
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Immunol Rev ; : — Nat Immunol ; 2 : — Immunity ; 43 : — Nat Immunol ; 17 : — Thymus-derived regulatory T cells are positively selected on natural self-antigen through cognate interactions of high functional avidity. Immunity ; 44 : — Aire enforces immune tolerance by directing autoreactive T cells into the regulatory T cell lineage.
Aire controls gene expression in the thymic epithelium with ordered stochasticity. Nat Immunol ; 16 : — Immune tolerance. Regulatory T cells generated early in life play a distinct role in maintaining self-tolerance. Nat Commun ; 7 : Development of T-cell tolerance utilizes both cell-autonomous and cooperative presentation of self-antigen.
Oh J, Shin JS. The role of dendritic cells in central tolerance. Immune Netw ; 15 : — Thymic B cells are licensed to present self antigens for central T cell tolerance induction. Immunity ; 42 : — Clonal deletion of thymocytes by circulating dendritic cells homing to the thymus. Nat Immunol ; 7 : — A wave of regulatory T cells into neonatal skin mediates tolerance to commensal microbes. T cell receptor reversed polarity recognition of a self-antigen major histocompatibility complex. Reversed T cell receptor docking on a major histocompatibility class I complex limits involvement in the immune response.
Immunity ; 45 : — J Exp Med ; : —42, S1. Neuropilin-1 distinguishes natural and inducible regulatory T cells among regulatory T cell subsets in vivo. J Exp Med ; : — S1— Elkord E.
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Helios should not be cited as a marker of human thymus-derived Tregs. Front Immunol ; 7 : Peripheral education of the immune system by colonic commensal microbiota.
Market economies need clear rules to function efficiently. Congress would approve the full package of recommendations via joint resolution. The generation of pTreg cells is even less clear than that of tTreg cells. The precise regulation of gene expression is necessary for organismal development, and changes in gene expression regulation underlie many evolutionary adaptations. Where appropriate promote regulatory coherence through co-ordination mechanisms between the supra national, the national and sub-national levels of government.
Thymus-derived regulatory T cells contribute to tolerance to commensal microbiota. Requirement of full TCR repertoire for regulatory T cells to maintain intestinal homeostasis.
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