Document Detail


IL-6 signaling SOCS critical for IL-12 host response to Toxoplasma gondii.
MedLine Citation:
PMID:  22191442     Owner:  NLM     Status:  In-Data-Review    
Abstract/OtherAbstract:
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.
Authors:
Julie Mirpuri; Felix Yarovinsky
Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Future microbiology     Volume:  7     ISSN:  1746-0921     ISO Abbreviation:  Future Microbiol     Publication Date:  2012 Jan 
Date Detail:
Created Date:  2011-12-23     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101278120     Medline TA:  Future Microbiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  13-6     Citation Subset:  IM    
Affiliation:
Department of Immunology, University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Boulevard, Dallas, TX 75390-9093, USA. felix.yarovinsky@utsouthwestern.edu.
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