The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.
Cutting Edge: IL-10-Independent STAT3 Activation by Toxoplasma gondii Mediates Suppression of IL-12 and TNF-α in Host Macrophages
Open accessAbstract
Infection of mouse macrophages by Toxoplasma gondii renders the cells resistant to proinflammatory effects of LPS triggering. In this study, we show that cell invasion is accompanied by rapid and sustained activation of host STAT3. Activation of STAT3 did not occur with soluble T. gondii extracts or heat-killed tachyzoites, demonstrating a requirement for live parasites. Parasite-induced STAT3 phosphorylation and suppression of LPS-triggered TNF-α and IL-12 was intact in IL-10-deficient macrophages, ruling out a role for this anti-inflammatory cytokine in the suppressive effects of T. gondii. Most importantly, Toxoplasma could not effectively suppress LPS-triggered TNF-α and IL-12 synthesis in STAT3-deficient macrophages. These results demonstrate that T. gondii exploits host STAT3 to prevent LPS-triggered IL-12 and TNF-α production, revealing for the first time a molecular mechanism underlying the parasite’s suppressive effect on macrophage proinflammatory cytokine production.
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Cites
Interleukin-10 and the Interleukin-10 Receptor
Moore, K. W., de Waal Malefyt, R., Coffman, R. L., & O'Garra, A. (2001) · Annual Review of Immunology · doi:10.1146/annurev.immunol.19.1.683 · Cited by 6,737
Enhanced DNA-Binding Activity of a Stat3-Related Protein in Cells Transformed by the Src Oncoprotein
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SOCS3 negatively regulates IL-6 signaling in vivo
Croker, B. A., Krebs, D. L., Zhang, J.-G., Wormald, S., Willson, T. A., Stanley, E. G., Robb, L., Greenhalgh, C. J., Förster, I., Clausen, B. E., et al. (2003) · Nature Immunology · doi:10.1038/ni931 · Cited by 840
IL-6 induces an anti-inflammatory response in the absence of SOCS3 in macrophages
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SOCS3 regulates the plasticity of gp130 signaling
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Cited by
SOCS proteins, cytokine signalling and immune regulation
Yoshimura, A., Naka, T., & Kubo, M. (2007) · Nature Reviews Immunology · doi:10.1038/nri2093 · Cited by 1,580
Toxoplasma co-opts host gene expression by injection of a polymorphic kinase homologue
Saeij, J. P. J., Coller, S., Boyle, J. P., Jerome, M. E., White, M. W., & Boothroyd, J. C. (2007) · Nature · doi:10.1038/nature05395 · Cited by 585
Understanding and exploiting the endogenous interleukin-10/STAT3-mediated anti-inflammatory response
MURRAY, P. (2006) · Current Opinion in Pharmacology · doi:10.1016/j.coph.2006.01.010 · Cited by 436
Self-citationGeneral nature of the STAT3-activated anti-inflammatory response.
El Kasmi, K. C., Holst, J., Coffre, M., Mielke, L., de Pauw, A., Lhocine, N., Smith, A. M., Rutschman, R., Kaushal, D., Shen, Y., et al. (2006) · The Journal of Immunology · doi:10.4049/jimmunol.177.11.7880 · Cited by 225
Self-citationInnate responses to Toxoplasma gondii in mice and humans
Pifer, R., & Yarovinsky, F. (2011) · Trends in Parasitology · doi:10.1016/j.pt.2011.03.009 · Cited by 139
Metadata
- Authors
- Butcher, B. A., Kim, L., Panopoulos, A. D., Watowich, S. S., Murray, P. J., & Denkers, E. Y.
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2005-03
- Volume
- 174
- Issue
- 6
- Pages
- 3148-3152
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W1953607369
- Cited by
- 160
- References
- 6
- FWCI
- 9.23
- Type
- journal article
- Language
- en
- Open access
- bronze
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- CoChat. (2026). Citation check: Cutting Edge: IL-10-Independent STAT3 Activation by Toxoplasma gondii Mediates Suppression of IL-12 and TNF-α in Host Macrophages. https://app.cochat.ai/papers/10.4049/jimmunol.174.6.3148
- The paper
- Butcher, B. A., Kim, L., Panopoulos, A. D., Watowich, S. S., Murray, P. J., & Denkers, E. Y. (2005). Cutting Edge: IL-10-Independent STAT3 Activation by Toxoplasma gondii Mediates Suppression of IL-12 and TNF-α in Host Macrophages. The Journal of Immunology. https://doi.org/10.4049/jimmunol.174.6.3148
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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