| IL-6 signaling SOCS critical for IL-12 host response to Toxoplasma gondii. | |
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MedLine Citation:
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PMID: 22191442 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
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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. |
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Authors:
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Julie Mirpuri; Felix Yarovinsky |
Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Future microbiology Volume: 7 ISSN: 1746-0921 ISO Abbreviation: Future Microbiol Publication Date: 2012 Jan |
Date Detail:
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Created Date: 2011-12-23 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 101278120 Medline TA: Future Microbiol Country: England |
Other Details:
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Languages: eng Pagination: 13-6 Citation Subset: IM |
Affiliation:
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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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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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