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Editor-in-Charge | How Xi
distributes the necessary and limited sources of energy and carbon is one of
the metabolic laws that the body needs to follow to establish a strong and efficient acquired immune response.
Metabolism must be tightly controlled at the cellular level to coordinate the expansion and differentiation
of T cells.
In addition to acting as bioenergy substrates and precursors to biosynthesis, metabolites can also directly control cellular signaling responses
by influencing DNA/RNA/protein modification, signal receptor activity, and reactive oxygen species production.
Therefore, metabolism is the basis for regulating carbon and nitrogen allocation and optimizing the immune response, and is also at the heart of
many diseases.
γ-aminobutyric acid (GAB) is its (GABA) biochemical form at physiological pH and serves as the underlying neurotransmitter of the central nervous system (CNS) in vertebrates, and its neuroexcitatory properties are clinically used to treat epilepsy
.
There is growing evidence that GAB may mediate cell-to-cell communication and act on various physiological processes
.
More importantly, as a traditional central neurotransmitter, its metabolic capacity also plays a role
in the immune response.
At present, GAB, as an important paracrine signaling molecule in the central nervous system, needs to be better explored, revealed and used in immune cells to provide a practical and reasonable method
for the treatment of inflammatory diseases and autoimmune diseases.
On October 3, 2022, the research team of Professor Ruoning Wang of the Nationwide Children's Hospital Research Center published a γ-aminobutyrate (GAB) functions as a bioenergetic and in Nature Metabolism Signaling gatekeeper to control T cell inflammation research article
.
The results revealed that the central neurotransmitter GAB functionally regulates T cell inflammation through bioenergetic and signal-controlled control
.
The study compares the extracellular metabolome profiles of different subsets of naïve T cells (naïve T, Tnai) and effector T cells (Teff), including helper T cells (T H0, TH1, TH), by first analyzing the extracellular metabolome, stable isotope tracking metabolic pathway analysis, and metabolic transcriptome 17) and inducible regulatory T cells (iTreg).
Finding that in helper (CD4+) pro-inflammatory T cells (TH17) and inducible regulatory T cells (iTreg) (Figure 1), GAB is one of
the most abundant metabolites produced by glutamine and arginine catabolism.
Further research has found that GAB plays a role
in controlling the control of biological energy and signal transmission through different mechanisms to control the differentiation of pro-inflammatory TH17cells and anti-inflammatory iTreg cells.
4-Aminobutyric acid aminotransferase (ABAT) introduces GAB as a chimeric substrate into the tricarboxylic acid (TCA) cycle to maximize carbon allocation to promote TH17cell differentiation
.
In contrast, in the absence of ABAT in iTreg cells, GAB can be secreted into the extracellular environment and facilitates iTreg cell differentiation
as an autocrine signaling metabolite.
Thus, knocking out or inhibiting the expression of ABAT in TH17cells can improve the pathogenic progression
of experimental autoimmune encephalomyelitis (EAE).
Conversely, knockout of GABA(A) receptors (GABAaR) in T cells exacerbates the pathogenic process
of EAE.
Overall, our results suggest that GAB's autonomic regulation of CD4+ T cells in the immune system as a traditional central neurotransmitter is bidirectional, relying on ABAT-mediated mitochondrial chimeralization and GABAaR regulated signaling responses (Figure 2).
Figure 1.
GAB is metabolically rich
in TH17and iTreg cells in Figure 2.
GAB bidirectional regulation
of pro-inflammatory TH17/anti-inflammatory iT reg by ABAT and GABAaR The results of this study elucidate previously unrecognized intrinsic effects ofT cells conferred by GAB catabolism and receptor-mediated signaling
.
In summary, GAB modulation strategies that block GAB catabolism, activate receptor-mediated responses, or combine both may be a promising therapy
for the treatment of inflammatory and autoimmune diseases.
Siwen Kang, a postdoc at the Nationwide Children's Hospital Research Center, is the first author of the paper, and Professor Ruoning Wang is the corresponding author
。 The paper is another important advance in the field of metabolism by Ruoning Wang's research group, which was previously reported by BioArt: Nat Metab | Inosine can be used as an alternative energy source for CD8+ T cells in glucose restriction and as | Sci Adv De de forma synthesis and salvage pathways coordinate the regulation of polyamine homeostasis to regulate T cell proliferation and function
.
Plate Maker: Eleven
distributes the necessary and limited sources of energy and carbon is one of
the metabolic laws that the body needs to follow to establish a strong and efficient acquired immune response.
Metabolism must be tightly controlled at the cellular level to coordinate the expansion and differentiation
of T cells.
In addition to acting as bioenergy substrates and precursors to biosynthesis, metabolites can also directly control cellular signaling responses
by influencing DNA/RNA/protein modification, signal receptor activity, and reactive oxygen species production.
Therefore, metabolism is the basis for regulating carbon and nitrogen allocation and optimizing the immune response, and is also at the heart of
many diseases.
γ-aminobutyric acid (GAB) is its (GABA) biochemical form at physiological pH and serves as the underlying neurotransmitter of the central nervous system (CNS) in vertebrates, and its neuroexcitatory properties are clinically used to treat epilepsy
.
There is growing evidence that GAB may mediate cell-to-cell communication and act on various physiological processes
.
More importantly, as a traditional central neurotransmitter, its metabolic capacity also plays a role
in the immune response.
At present, GAB, as an important paracrine signaling molecule in the central nervous system, needs to be better explored, revealed and used in immune cells to provide a practical and reasonable method
for the treatment of inflammatory diseases and autoimmune diseases.
On October 3, 2022, the research team of Professor Ruoning Wang of the Nationwide Children's Hospital Research Center published a γ-aminobutyrate (GAB) functions as a bioenergetic and in Nature Metabolism Signaling gatekeeper to control T cell inflammation research article
.
The results revealed that the central neurotransmitter GAB functionally regulates T cell inflammation through bioenergetic and signal-controlled control
.
The study compares the extracellular metabolome profiles of different subsets of naïve T cells (naïve T, Tnai) and effector T cells (Teff), including helper T cells (T H0, TH1, TH), by first analyzing the extracellular metabolome, stable isotope tracking metabolic pathway analysis, and metabolic transcriptome 17) and inducible regulatory T cells (iTreg).
Finding that in helper (CD4+) pro-inflammatory T cells (TH17) and inducible regulatory T cells (iTreg) (Figure 1), GAB is one of
the most abundant metabolites produced by glutamine and arginine catabolism.
Further research has found that GAB plays a role
in controlling the control of biological energy and signal transmission through different mechanisms to control the differentiation of pro-inflammatory TH17cells and anti-inflammatory iTreg cells.
4-Aminobutyric acid aminotransferase (ABAT) introduces GAB as a chimeric substrate into the tricarboxylic acid (TCA) cycle to maximize carbon allocation to promote TH17cell differentiation
.
In contrast, in the absence of ABAT in iTreg cells, GAB can be secreted into the extracellular environment and facilitates iTreg cell differentiation
as an autocrine signaling metabolite.
Thus, knocking out or inhibiting the expression of ABAT in TH17cells can improve the pathogenic progression
of experimental autoimmune encephalomyelitis (EAE).
Conversely, knockout of GABA(A) receptors (GABAaR) in T cells exacerbates the pathogenic process
of EAE.
Overall, our results suggest that GAB's autonomic regulation of CD4+ T cells in the immune system as a traditional central neurotransmitter is bidirectional, relying on ABAT-mediated mitochondrial chimeralization and GABAaR regulated signaling responses (Figure 2).
Figure 1.
GAB is metabolically rich
in TH17and iTreg cells in Figure 2.
GAB bidirectional regulation
of pro-inflammatory TH17/anti-inflammatory iT reg by ABAT and GABAaR The results of this study elucidate previously unrecognized intrinsic effects ofT cells conferred by GAB catabolism and receptor-mediated signaling
.
In summary, GAB modulation strategies that block GAB catabolism, activate receptor-mediated responses, or combine both may be a promising therapy
for the treatment of inflammatory and autoimmune diseases.
Siwen Kang, a postdoc at the Nationwide Children's Hospital Research Center, is the first author of the paper, and Professor Ruoning Wang is the corresponding author
。 The paper is another important advance in the field of metabolism by Ruoning Wang's research group, which was previously reported by BioArt: Nat Metab | Inosine can be used as an alternative energy source for CD8+ T cells in glucose restriction and as | Sci Adv De de forma synthesis and salvage pathways coordinate the regulation of polyamine homeostasis to regulate T cell proliferation and function
.
Original link:
https://doi.
org/10.
1038/s42255-022-00638-1
Plate Maker: Eleven
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