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Complement Regulates Nutrient Influx and Metabolic Reprogramming during Th1 Cell Responses.

Martin Kolev1, Sarah Dimeloe2, Gaelle Le Friec1

  • 1Division of Transplant Immunology and Mucosal Biology, MRC Centre for Transplantation, King's College London, Guy's Hospital, Great Maze Pond, London SE1 9RT, UK.

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Summary
This summary is machine-generated.

The complement receptor CD46 (cytoplasmic domain 1) is crucial for T helper 1 (Th1) cell metabolic reprogramming, enhancing amino acid and glucose transport for effector function. This finding links the complement system to T cell metabolic adaptation and cytokine production.

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Area of Science:

  • Immunology
  • Cell Metabolism
  • Complement System

Background:

  • Th1 cell effector function relies on metabolic reprogramming, but the signals guiding this process are unclear.
  • Understanding these signals is vital for controlling T cell responses and immune function.

Purpose of the Study:

  • To investigate the role of the complement receptor CD46 in metabolic adaptations of human T cells.
  • To identify the specific CD46 signaling pathways involved in T cell metabolic reprogramming and effector function.

Main Methods:

  • Analysis of activated human T cells, including those from CD46-deficient patients.
  • Assessment of amino acid (AA) and glucose transporter expression (LAT1, GLUT1).
  • Evaluation of LAMTOR5 expression, Ragulator-Rag-mTORC1 complex assembly, glycolysis, and oxidative phosphorylation (OXPHOS).

Main Results:

  • CD46 (cytoplasmic domain 1) activation induced LAT1 and GLUT1 expression in human T cells.
  • CD46 promoted LAMTOR5 expression, facilitating mTORC1 complex assembly and increasing glycolysis and OXPHOS.
  • CD46-deficient T cells showed impaired metabolic reprogramming and reduced IFN-γ production, which was restored by CD46-CYT-1 expression.

Conclusions:

  • CD46 signaling is essential for the metabolic reprogramming required for human Th1 cell effector function.
  • This study establishes a critical link between complement activation and immunometabolic adaptations in T cells.
  • Targeting CD46 may offer therapeutic strategies for modulating T cell responses.