ArticleFuture microbiology2012
IL-6 signaling SOCS critical for IL-12 host response to Toxoplasma gondii.
Article in Future microbiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
6 citing papers in PubMed, 13 citations in OpenAlex.
- Biogenic Silver Nanoparticles Can ControlFrontiers in microbiology · 2020Article
- Enrofloxacin and Toltrazuril Are Able to ReduceFrontiers in cellular and infection microbiology · 2017Article
- Transcriptomic analysis of global changes in cytokine expression in mouse spleens following acute Toxoplasma gondii infection.Parasitology research · 2016Article
- Dectin-1-CD37 association regulates IL-6 expression during Toxoplasma gondii infection.Parasitology research · 2014Article
- SOCS proteins in infectious diseases of mammals.Veterinary immunology and immunopathology · 2013Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.