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Sulfur is an essential element in biological systems, contributing to synthesizing key biomolecules, including amino acids such as cysteine and methionine, and cofactors such as coenzyme A and biotin. Microorganisms primarily assimilate sulfur as sulfate (SO₄²⁻) from the environment, which must undergo a series of biochemical transformations before it can be incorporated into cellular components. As sulfate is highly oxidized, it must undergo assimilatory sulfate reduction to...
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When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
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Sulfur is a vital element in Earth's biogeochemical systems. It transitions through various inorganic states, including sulfate (SO₄²⁻), elemental sulfur (S⁰), and sulfide (S²⁻). Abiotic and biological mechanisms across oxic and anoxic environments intricately mediate these transformations. Sulfate, the most oxidized form of sulfur, is predominantly stored in rocks, marine sediments, and oceanic waters, acting as a long-term reservoir in the global sulfur...
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Sulfur partitioning from cysteine controls T cell proliferation and effector function.

Beth Kelly1, Minsun Cha1, Tatjana Gremelspacher1

  • 1Bloomberg-Kimmel Institute of Immunotherapy, Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.

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Summary

CD8+ T cells use cysteine for glutathione production and iron-sulfur cluster synthesis. Manipulating these pathways impacts T cell function and anti-cancer immunity, offering new therapeutic strategies.

Keywords:
CD8+ T cellsFe-S clustersT cell exhaustionanti-tumor immunitycysteineglutathioneimmunometabolismiron uptakelipid peroxidationmitochondria

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Area of Science:

  • Immunology
  • Cell Metabolism
  • Biochemistry

Background:

  • Understanding nutrient utilization in T cells is crucial for immune function.
  • The specific roles of cysteine in CD8+ T cell metabolism and function require further elucidation.

Purpose of the Study:

  • To investigate how CD8+ T cells partition acquired cysteine into distinct intracellular metabolic pathways.
  • To determine the functional consequences of cysteine's metabolic fates on T cell effector functions and anti-cancer immunity.

Main Methods:

  • Utilized NFS1 deletion in activated CD8+ T cells.
  • Investigated the effects of blocking cysteine flux into glutathione (GSH).
  • Analyzed the impact of enforcing iron-sulfur (FeS) metabolism.

Main Results:

  • Cysteine serves as a substrate for GSH production, modulating effector functions.
  • Cysteine's sulfur is used for NFS1-dependent FeS cluster synthesis, supporting proliferation.
  • NFS1 deletion in T cells promotes exhaustion and dampens anti-cancer immunity.
  • Blocking GSH or enforcing FeS metabolism impacts tumor control.
  • Disrupted FeS metabolism in T cells correlates with exhaustion in human hepatocellular carcinoma.

Conclusions:

  • Targeted control of cysteine flux can modulate T cell function and anti-cancer immunity.
  • Cysteine metabolism plays a critical role in T cell proliferation, effector functions, and exhaustion.
  • Findings suggest potential therapeutic strategies by manipulating cysteine metabolic pathways for enhanced anti-cancer immunity.