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Updated: May 26, 2026

Forward Genetics Screens Using Macrophages to Identify Toxoplasma gondii Genes Important for Resistance to IFN-γ-Dependent Cell Autonomous Immunity
Published on: March 12, 2015
IL-6 signaling SOCS critical for IL-12 host response to Toxoplasma gondii
Julie Mirpuri1, Felix Yarovinsky
1Department of Immunology, University of Texas Southwestern Medical Center at Dallas, Dallas, TX 75390-9093, USA.
Abstract:
SOCS are a family of proteins that play an important role in the negative regulation of the cytokine-JAK-STAT pathway. Socs3 deletion results in prolonged IL-6 signaling measured by STAT3 phosphorylation. A role for STAT3 and SOCS3 in the context of Toxoplasma gondii infection is of particular importance, because STAT3 appears to be a key target of T. gondii virulence factors. By utilizing LysM-cre Socs3(fl/fl) mice, the Hunter laboratory recently established that macrophage-specific SOCS3 knockout mice have enhanced susceptibility to infection with T. gondii. The authors demonstrated that lack of SOCS3-mediated control of IL-6 signaling results in acute susceptibility to T. gondii due to impaired IL-12 production by inflammatory monocytes, macrophages and neutrophils. This article further explores these findings and their implications in the field of host resistance to microbial pathogens.
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