The DOI matches its Crossref record; 56 of the 56 references it cites were found in a registry or an index.
MyD88 inhibition amplifies dendritic cell capacity to promote pancreatic carcinogenesis via Th2 cells
Open accessAbstract
The transition of chronic pancreatic fibroinflammatory disease to neoplasia is a primary example of the paradigm linking inflammation to carcinogenesis. However, the cellular and molecular mediators bridging these entities are not well understood. Because TLR4 ligation can exacerbate pancreatic inflammation, we postulated that TLR4 activation drives pancreatic carcinogenesis. In this study, we show that lipopolysaccharide accelerates pancreatic tumorigenesis, whereas TLR4 inhibition is protective. Furthermore, blockade of the MyD88-independent TRIF pathway is protective against pancreatic cancer, whereas blockade of the MyD88-dependent pathway surprisingly exacerbates pancreatic inflammation and malignant progression. The protumorigenic and fibroinflammatory effects of MyD88 inhibition are mediated by dendritic cells (DCs), which induce pancreatic antigen–restricted Th2-deviated CD4+ T cells and promote the transition from pancreatitis to carcinoma. Our data implicate a primary role for DCs in pancreatic carcinogenesis and illustrate divergent pathways in which blockade of TLR4 signaling via TRIF is protective against pancreatic cancer and, conversely, MyD88 inhibition exacerbates pancreatic inflammation and neoplastic transformation by augmenting the DC–Th2 axis.
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1 retracted
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Cancer-related inflammation, the seventh hallmark of cancer: links to genetic instability
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Cited by
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Self-citationGenetics and biology of pancreatic ductal adenocarcinoma
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Gut microbiota-mediated inflammation in obesity: a link with gastrointestinal cancer
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Metadata
- Authors
- Ochi, A., Nguyen, A. H., Bedrosian, A. S., Mushlin, H. M., Zarbakhsh, S., Barilla, R., Zambirinis, C. P., Fallon, N. C., Rehman, A., Pylayeva-Gupta, Y., Badar, S., Hajdu, C. H., Frey, A. B., Bar-Sagi, D., & Miller, G.
- Venue
- Journal of Experimental Medicine
- Publisher
- Rockefeller University Press
- Published
- 2012-08-20
- Volume
- 209
- Issue
- 9
- Pages
- 1671-1687
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- OpenAlex
- W2153042210
- Cited by
- 304
- References
- 56
- FWCI
- 7.81
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Ochi, A., Nguyen, A. H., Bedrosian, A. S., Mushlin, H. M., Zarbakhsh, S., Barilla, R., Zambirinis, C. P., Fallon, N. C., Rehman, A., Pylayeva-Gupta, Y., Badar, S., Hajdu, C. H., Frey, A. B., Bar-Sagi, D., & Miller, G. (2012). MyD88 inhibition amplifies dendritic cell capacity to promote pancreatic carcinogenesis via Th2 cells. Journal of Experimental Medicine. https://doi.org/10.1084/jem.20111706
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
