ArticleThe Journal of experimental medicine2011
Strain-specific activation of the NF-kappaB pathway by GRA15, a novel Toxoplasma gondii dense granule protein.
Article in The Journal of experimental medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 274 papers, 1 of them a synthesis that pooled it.
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Who cites it
274 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Is Toxoplasma gondii type related to clinical outcome in human congenital infection? Systematic and critical review.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2016Pooled it
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- Toxoplasma gondii as a drug for anti-tumor immunotherapy: mechanisms, challenges, and perspectives.Parasite (Paris, France) · 2026Review
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- GRA86 Is a Novel Dense Granule Protein Important for Virulence and Bradyzoite Differentiation inAnimals : an open access journal from MDPI · 2025Article
214 more citing papers are in PubMed but not listed here.
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7 authors.
Funding
Abstract
NF-κB is an integral component of the immune response to Toxoplasma gondii. Although evidence exists that T. gondii can directly modulate the NF-κB pathway, the parasite-derived effectors involved are unknown. We determined that type II strains of T. gondii activate more NF-κB than type I or type III strains, and using forward genetics we found that this difference is a result of the polymorphic protein GRA15, a novel dense granule protein which T. gondii secretes into the host cell upon invasion. A GRA15-deficient type II strain has a severe defect in both NF-κB nuclear translocation and NF-κB-mediated transcription. Furthermore, human cells expressing type II GRA15 also activate NF-κB, demonstrating that GRA15 alone is sufficient for NF-κB activation. Along with the rhoptry protein ROP16, GRA15 is responsible for a large part of the strain differences in the induction of IL-12 secretion by infected mouse macrophages. In vivo bioluminescent imaging showed that a GRA15-deficient type II strain grows faster compared with wild-type, most likely through its reduced induction of IFN-γ. These results show for the first time that a dense granule protein can modulate host signaling pathways, and dense granule proteins can therefore join rhoptry proteins in T. gondii's host cell-modifying arsenal.
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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.