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SOTA/Thematic

How T cell metabolism regulates function and survival

Carl Atkinson
Presenter
Carl Atkinson (US)

Professor · Department of Surgery · Northwestern University · Chicago

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Overview

T-cell activation requires profound metabolic reprogramming to support proliferation, cytokine production, and effector function. This session will examine how these metabolic programs shape alloimmune responses in solid organ transplantation, how the metabolically injured graft may further amplify T-cell activation, and how emerging strategies targeting glycolysis, glutamine metabolism, mitochondrial function, and other metabolic checkpoints could be used to control rejection and promote immune regulation.

Learning Objectives

  • Describe how T-cell metabolic reprogramming supports activation, differentiation, and effector function during alloimmunity.
  • Explain how the metabolically injured graft can shape and amplify T-cell responses through changes in nutrients, metabolites, hypoxia, and inflammatory signaling.
  • Identify key metabolic pathways currently being targeted in transplantation, including glycolysis, glutamine metabolism, mitochondrial function, one-carbon metabolism, and polyamine synthesis.
  • Discuss how selective manipulation of T-cell metabolism could suppress rejection while preserving regulation, protective immunity, and potentially promoting graft tolerance