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Transcriptome and proteome expression in activated human CD4 and CD8 T-lymphocytes.
Frankie B Stentz1, Abbas E Kitabchi
1Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, The University of Tennessee Health Science Center, Memphis, TN, USA. fstentz@utmem.edu
Biochemical and Biophysical Research Communications
|October 12, 2004
Summary
Activated T-cells gain insulin receptors, becoming insulin sensitive. This study reveals gene expression changes in activated T-cells, offering insights into their metabolic roles in conditions like diabetic ketoacidosis.
Area of Science:
- Immunology
- Endocrinology
- Genomics
- Proteomics
Background:
- T-lymphocytes (T-cells) are typically insulin-insensitive due to a lack of insulin receptors.
- Antigen activation induces insulin, IGF-1, and IL-2 receptor expression on T-cells, rendering them insulin-sensitive.
- In vivo T-cell activation has been observed in patients with diabetic ketoacidosis.
Purpose of the Study:
- To investigate the genomic and proteomic changes in activated versus non-activated T-cells.
- To identify specific genes and pathways affected by T-cell activation.
- To explore the physiological significance of these T-cell alterations.
Main Methods:
- Analysis of genomics using Affymetrix microarray gene chips.
- Proteomics analysis using SELDI-TOF mass spectrometry.
- Evaluation of approximately 27,000 genes across various cellular ontologies.
Main Results:
- Genes for IL-2, insulin, and IGF-1 receptors were significantly upregulated (at least 2-fold) in activated T-cells.
- Approximately 10,500 genes were increased, while 7,000 were decreased in activated T-cells.
- Activated ontologies included key signal transduction pathways (IRS-1, IRS-2, Akt) and glycolytic pathways.
Conclusions:
- T-cell activation leads to the development of insulin receptors and sensitivity.
- Genomic and proteomic analyses reveal widespread gene expression changes, including metabolic pathways, upon T-cell activation.
- This study presents novel findings on T-cell activation and its potential physiological implications, particularly in metabolic contexts.