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Cited by 674

The DOI matches its Crossref record; 49 of the 49 references it cites were found in a registry or an index.

Aryl hydrocarbon receptor control of a disease tolerance defence pathway

Open access
Bessede, Alban, Gargaro, Marco, Pallotta, Maria T., Matino, Davide, Servillo, Giuseppe, Brunacci, Cinzia, Bicciato, Silvio, Mazza, Emilia M. C., Macchiarulo, Antonio, Vacca, Carmine, Iannitti, Rossana, Tissi, Luciana, Volpi, Claudia, Belladonna, Maria L., Orabona, Ciriana, Bianchi, Roberta, Lanz, Tobias V., Platten, Michael, Della Fazia, Maria A., Piobbico, Danilo, Zelante, Teresa, Funakoshi, Hiroshi, Nakamura, Toshikazu, Gilot, David, Denison, Michael S., Guillemin, Gilles J., DuHadaway, James B., Prendergast, George C., Metz, Richard, Geffard, Michel, Boon, Louis, Pirro, Matteo, Iorio, Alfonso, Veyret, Bernard, Romani, Luigina, Grohmann, Ursula, Fallarino, Francesca, Puccetti, Paolo·2014·Nature

Abstract

Disease tolerance is the ability of the host to reduce the effect of infection on host fitness. Analysis of disease tolerance pathways could provide new approaches for treating infections and other inflammatory diseases. Typically, an initial exposure to bacterial lipopolysaccharide (LPS) induces a state of refractoriness to further LPS challenge (endotoxin tolerance). We found that a first exposure of mice to LPS activated the ligand-operated transcription factor aryl hydrocarbon receptor (AhR) and the hepatic enzyme tryptophan 2,3-dioxygenase, which provided an activating ligand to the former, to downregulate early inflammatory gene expression. However, on LPS rechallenge, AhR engaged in long-term regulation of systemic inflammation only in the presence of indoleamine 2,3-dioxygenase 1 (IDO1). AhR-complex-associated Src kinase activity promoted IDO1 phosphorylation and signalling ability. The resulting endotoxin-tolerant state was found to protect mice against immunopathology in Gram-negative and Gram-positive infections, pointing to a role for AhR in contributing to host fitness.

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Metadata

Authors
Bessede, A., Gargaro, M., Pallotta, M. T., Matino, D., Servillo, G., Brunacci, C., Bicciato, S., Mazza, E. M. C., Macchiarulo, A., Vacca, C., Iannitti, R., Tissi, L., Volpi, C., Belladonna, M. L., Orabona, C., Bianchi, R., Lanz, T. V., Platten, M., Della Fazia, M. A., Piobbico, D., Zelante, T., Funakoshi, H., Nakamura, T., Gilot, D., Denison, M. S., Guillemin, G. J., DuHadaway, J. B., Prendergast, G. C., Metz, R., Geffard, M., Boon, L., Pirro, M., Iorio, A., Veyret, B., Romani, L., Grohmann, U., Fallarino, F., & Puccetti, P.
Venue
Nature
Published
2014-07-09
Volume
511
Issue
7508
Pages
184-190
ISSN
  • 0028-0836 (ISSN-L)
  • 1476-4687
OpenAlex
W2008343182
Cited by
674
References
49
FWCI
24.77
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: Aryl hydrocarbon receptor control of a disease tolerance defence pathway. https://app.cochat.ai/papers/10.1038/nature13323
The paper
Bessede, A., Gargaro, M., Pallotta, M. T., Matino, D., Servillo, G., Brunacci, C., Bicciato, S., Mazza, E. M. C., Macchiarulo, A., Vacca, C., Iannitti, R., Tissi, L., Volpi, C., Belladonna, M. L., Orabona, C., Bianchi, R., Lanz, T. V., Platten, M., Della Fazia, M. A., . . . Puccetti, P. (2014). Aryl hydrocarbon receptor control of a disease tolerance defence pathway. Nature. https://doi.org/10.1038/nature13323

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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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