IFN-gamma production during active tuberculosis is regulated by mechanisms that involve IL-17, SLAM, and CREB.
basic_science · Level V
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- Record sourced from PubMed, PMID 19199539.
- Also identified by DOI 10.1086/596742 and PMC identifier 5488291.
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Abstract
Interferon-gamma (IFN-gamma) is crucial for protection against Mycobacterium tuberculosis, and the transcription factor cAMP response element binding protein (CREB) increases IFN-gamma transcription. We determined whether the transmembrane receptor signaling lymphocyte activation molecule (SLAM) and interleukin-17 (IL-17) affect CREB phosphorylation and IFN-gamma production in persons with tuberculosis. When T cells from patients with tuberculosis were activated with M. tuberculosis, 80% of SLAM(+) T cells expressed phosphorylated CREB, and SLAM activation increased CREB phosphorylation and IFN-gamma production. In contrast, IL-17 down-regulated SLAM expression, CREB phosphorylation, and IFN-gamma production. Therefore, IL-17 and SLAM have opposing effects on IFN-gamma production through CREB activation in persons with tuberculosis.
Medical subject headings
- Antigens, CD
- Cyclic AMP Response Element-Binding Protein
- Interferon-gamma
- Interleukin-17
- Receptors, Cell Surface
- Tuberculosis