Releasing the Brake on IFN-γ Signaling on Infection

Carsten G K Lüder; Kristina Sumpf; Roswitha Nast

doi:10.1016/j.pt.2015.08.006

Releasing the Brake on IFN-γ Signaling on Infection

Trends Parasitol. 2015 Oct;31(10):456-459. doi: 10.1016/j.pt.2015.08.006. Epub 2015 Sep 30.

Authors

Carsten G K Lüder¹, Kristina Sumpf², Roswitha Nast²

Affiliations

¹ Institute for Medical Microbiology, Georg August University, Göttingen, Germany. Electronic address: clueder@gwdg.de.
² Institute for Medical Microbiology, Georg August University, Göttingen, Germany.

PMID: 26422772
DOI: 10.1016/j.pt.2015.08.006

Abstract

Toxoplasma gondii effectively inhibits the responsiveness of its host cell to interferon gamma (IFN-γ). Using a genome-wide genetic screen, Beiting and colleagues have recently identified coactivators of the transcription factor STAT1 that can diminish this inhibitory effect. One of these coactivators, TLX, enhances type 1 helper (Th1) immune responses and restricts parasite replication during chronic toxoplasmosis.

Keywords: IFN-γ; STAT1; TLX; Toxoplasma gondii; parasite–host interaction; transcription.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Animals
Genome-Wide Association Study
Host-Parasite Interactions / genetics
Host-Parasite Interactions / immunology*
Humans
Interferon-gamma / metabolism*
Receptors, Cytoplasmic and Nuclear / genetics
Receptors, Cytoplasmic and Nuclear / metabolism
STAT1 Transcription Factor / genetics
STAT1 Transcription Factor / metabolism
Signal Transduction / genetics
Signal Transduction / immunology*
Th1 Cells / immunology
Th1 Cells / parasitology
Toxoplasma / immunology
Toxoplasmosis / immunology*

Substances

Receptors, Cytoplasmic and Nuclear
STAT1 Transcription Factor
Interferon-gamma