Monocarboxylate transporter 1 deficiency impacts CD8 + T lymphocytes proliferation and recruitment to adipose tissue during obesity

C Macchi
Università degli Studi di Milano
January 1, 2022
iScience
https://pubmed.ncbi.nlm.nih.gov/35707720

This article is currently being updated. View its version on PubMed.

https://pubmed.ncbi.nlm.nih.gov/35707720

Research summary

This study investigates the role of monocarboxylate transporter 1 (MCT1) in CD8⁺ T cell function during obesity-induced inflammation. Using a T cell-specific Slc16a1 (MCT1) Knockout mouse model, researchers found that MCT1 deficiency impairs CD8⁺ T cell proliferation and alters their metabolic programming, leading to reduced recruitment to adipose tissue and decreased adipose tissue inflammation during high-fat diet-induced obesity.

Key outcome of the study

MCT1 deficiency in T cells impairs CD8⁺ T cell proliferation and recruitment to adipose tissue, leading to reduced adipose tissue inflammation during obesity.

Model

T cell-specific Slc16a1 (MCT1) conditional Knockout mouse model (Slc16a1^flox/flox; CD4-Cre), developed to study the impact of MCT1 deficiency in T cells during obesity.

TARGET:
Slc16a1
Synonyms:
MCT1, Monocarboxylate transporter 1

Keywords

Obesity, T cell metabolism, Adipose tissue inflammation, Immunometabolism

Technical specifications

Conditional Knockout, CD4-Cre, T cell-specific gene deletion, Metabolic reprogramming

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