Glutamine restrains T cell pathogenicity in MASLD

Chendi Yang; Eyad Elkord; Weiwei Dai

Glutamine restrains T cell pathogenicity in MASLD

Chendi Yang
, Eyad Elkord^*
, Weiwei Dai^*

^*Corresponding author for this work

Oncology and Immunology

Research output: Contribution to journal › Article › peer-review

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Abstract

How does glutamine metabolism shape pathogenic CD4+ T cell responses in MASLD? Sawada et al. recently showed that glutamine supplementation limits liver injury, while T-cell-intrinsic GLS1-mediated glutaminolysis restrains inflammatory output, implicating O-GlcNAcylation as a candidate link. These findings revealed that glutamine metabolism can restrain, rather than simply fuel, T-cell pathogenicity.

Original language	English
Article number	TEM-D-26-00677
Journal	Trends in Endocrinology and Metabolism
Publication status	Submitted - 2 Oct 2026

Keywords

Glutamine
T cell
MASLD

Access to Document

TEM-D-26-00677Submitted manuscript, 78.1 KBLicence: CC BY-ND

Cite this

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title = "Glutamine restrains T cell pathogenicity in MASLD",

abstract = "How does glutamine metabolism shape pathogenic CD4+ T cell responses in MASLD? Sawada et al. recently showed that glutamine supplementation limits liver injury, while T-cell-intrinsic GLS1-mediated glutaminolysis restrains inflammatory output, implicating O-GlcNAcylation as a candidate link. These findings revealed that glutamine metabolism can restrain, rather than simply fuel, T-cell pathogenicity.",

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AU - Yang, Chendi

AU - Elkord, Eyad

AU - Dai, Weiwei

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N2 - How does glutamine metabolism shape pathogenic CD4+ T cell responses in MASLD? Sawada et al. recently showed that glutamine supplementation limits liver injury, while T-cell-intrinsic GLS1-mediated glutaminolysis restrains inflammatory output, implicating O-GlcNAcylation as a candidate link. These findings revealed that glutamine metabolism can restrain, rather than simply fuel, T-cell pathogenicity.

AB - How does glutamine metabolism shape pathogenic CD4+ T cell responses in MASLD? Sawada et al. recently showed that glutamine supplementation limits liver injury, while T-cell-intrinsic GLS1-mediated glutaminolysis restrains inflammatory output, implicating O-GlcNAcylation as a candidate link. These findings revealed that glutamine metabolism can restrain, rather than simply fuel, T-cell pathogenicity.

KW - Glutamine

KW - T cell

KW - MASLD

M3 - Article

SN - 1879-3061

JO - Trends in Endocrinology and Metabolism

JF - Trends in Endocrinology and Metabolism

M1 - TEM-D-26-00677

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