Sunday, December 25, 2011

IL-6 signaling SOCS critical for IL-12 host response to Toxoplasma gondii

Future Microbiol. 2012 Jan;7:13-6.

IL-6 signaling SOCS critical for IL-12 host response to Toxoplasma gondii.

Mirpuri J, Yarovinsky F.


Department of Immunology, University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Boulevard, Dallas, TX 75390-9093, USA.


Evaluation of: Whitmarsh RJ, Gray CM, Gregg B et al. A critical role for SOCS3 in innate resistance to Toxoplasma gondii. Cell Host Microbe 10(3), 224-236 (2011). 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.

PMID: 22191442 [PubMed - in process]

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