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GLUT‐1 transporter expression is up‐regulated on human CD4+ and CD8+ T lymphocytes following T cell activation
Author(s) -
MENG HUICUI,
TURBITT WILLIAM J,
ROGERS CONNIE J
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1027.15
Subject(s) - cd28 , glucose transporter , t cell , cd8 , flow cytometry , biology , il 2 receptor , cytotoxic t cell , immune system , microbiology and biotechnology , chemistry , immunology , endocrinology , insulin , biochemistry , in vitro
The availability and uptake of nutrients play a critical role in the generation of adequate immune responses. In particular, the metabolic demands of T lymphocytes increase following activation to provide energy for proliferation and other important effector functions. Glucose, one of the major energy sources of T cells, can be transported into cells via several glucose transporters, including GLUT‐1. However, the distribution of GLUT‐1 on T cell subsets remains unclear. Therefore, the goal of the current study was to evaluate the effect of T cell activation on GLUT‐1 expression in CD4 + and CD8 + T cells. Peripheral blood was collected from healthy subjects (20–40 years old), PBMCs were isolated using Ficoll‐Hypaque Plus, and T cells were stimulated using 1 μg/ml of anti‐CD3/CD28 antibodies. Following 3‐day cultures, T cells were harvested, counted and GLUT‐1 expression was quantified on both unactivated and activated CD4 + and CD8 + T cells by flow cytometry. GLUT‐1 expression increased significantly, on CD4 + and CD8 + T cells (20‐fold and 10‐fold, respectively; P<0.05) following activation. Our results demonstrate that CD4 + and CD8 + T cells up‐regulate the surface expression of GLUT‐1 upon activation. These results suggest that increased glucose uptake via the GLUT‐1 transporter is a common feature of all activated T cells and may be a target for therapy to enhance T cell function. Grant Funding Source : Penn State internal funding