IFN-gamma production during active tuberculosis is regulated by mechanisms that involve IL-17, SLAM, and CREB

J Infect Dis. 2009 Mar 1;199(5):661-5. doi: 10.1086/596742.

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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antigens, CD / genetics
  • Antigens, CD / metabolism*
  • Cyclic AMP Response Element-Binding Protein / genetics
  • Cyclic AMP Response Element-Binding Protein / metabolism*
  • Gene Expression Regulation, Bacterial / physiology
  • Humans
  • Interferon-gamma / metabolism*
  • Interleukin-17 / genetics
  • Interleukin-17 / metabolism*
  • Phosphorylation
  • Receptors, Cell Surface / genetics
  • Receptors, Cell Surface / metabolism*
  • Signaling Lymphocytic Activation Molecule Family Member 1
  • Tuberculosis / immunology*
  • Tuberculosis / metabolism

Substances

  • Antigens, CD
  • CREB1 protein, human
  • Cyclic AMP Response Element-Binding Protein
  • Interleukin-17
  • Receptors, Cell Surface
  • Signaling Lymphocytic Activation Molecule Family Member 1
  • Interferon-gamma