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Related Experiment Video

Updated: Dec 24, 2025

Multicolor Flow Cytometry-based Quantification of Mitochondria and Lysosomes in T Cells

Multicolor Flow Cytometry-based Quantification of Mitochondria and Lysosomes in T Cells

Published on: January 9, 2019

T cell Metabolism in Lupus.

Milena Vukelic¹, Michihito Kono², George C Tsokos¹

¹Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA.

Immunometabolism

|April 8, 2020

Summary

Systemic lupus erythematosus involves abnormal T cell responses driven by metabolic reprogramming. Defects in mitochondrial function, glycolysis, and lipid metabolism contribute to inflammation, offering therapeutic targets.

Keywords:

SLE T cell metabolism fatty acid oxidation glutaminolysis glycolysis

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Measuring Mitochondrial Function of Naïve and Effector CD8 T Cells

Measuring Mitochondrial Function of Naïve and Effector CD8 T Cells

Published on: March 28, 2025

Area of Science:

Immunology
Metabolic pathways
Autoimmune diseases

Background:

T cell responses are crucial in systemic lupus erythematosus (SLE) pathogenesis.
Metabolic reprogramming, including glycolysis and mitochondrial function, influences T cell differentiation and function.
Dysregulated T cell metabolism is increasingly recognized in autoimmunity.

Purpose of the Study:

To review the role of metabolic defects in T cell dysfunction in SLE.
To explore how mitochondrial dysfunction, oxidative stress, glycolysis, glutaminolysis, and lipid metabolism contribute to pro-inflammatory T cell responses in SLE.
To discuss potential therapeutic strategies targeting metabolic pathways in SLE.

Main Methods:

Literature review and synthesis of existing research on T cell metabolism in SLE.
Analysis of the impact of specific metabolic pathways (e.g., glycolysis, glutaminolysis, lipid metabolism) on T cell function in autoimmunity.
Discussion of the interplay between metabolic defects and immune cell responses.

Main Results:

Abnormalities in mitochondrial function, oxidative stress, glycolysis, glutaminolysis, and lipid metabolism are linked to pro-inflammatory T cell responses in SLE.
Specific metabolic pathways, modulated by molecules like CD28, PD-1, and CTLA-4, impact T cell fate and function.
Metabolic reprogramming is a key feature of T cell dysfunction in SLE.

Conclusions:

Metabolic defects significantly contribute to the pathogenesis of systemic lupus erythematosus by promoting pro-inflammatory T cell responses.
Targeting metabolic pathways in T cells presents a promising therapeutic avenue for managing SLE.
Further research into T cell metabolism holds potential for novel SLE treatments.