The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.
IL‐23 and the Th17 pathway promote inflammation and impair antifungal immune resistance
Abstract
Although inflammation is an essential component of the protective response to fungi, its dysregulation may significantly worsen fungal diseases. We found here that the IL‐23/IL‐17 developmental pathway acted as a negative regulator of the Th1‐mediated immune resistance to fungi and played an inflammatory role previously attributed to uncontrolled Th1 cell responses. Both inflammation and infection were exacerbated by a heightened Th17 response against Candida albicans and Aspergillus fumigatus , two major human fungal pathogens. IL‐23 acted as a molecular connection between uncontrolled fungal growth and inflammation, being produced by dendritic cells in response to a high fungal burden and counter‐regulating IL‐12p70 production. Both IL‐23 and IL‐17 subverted the inflammatory program of neutrophils, which resulted in severe tissue inflammatory pathology associated with infection. Our data are the first demonstrating that the IL‐23/IL‐17 pathway promotes inflammation and susceptibility in an infectious disease model. As IL‐23‐driven inflammation promotes infection and impairs antifungal resistance, modulation of the inflammatory response represents a potential strategy to stimulate protective immune responses to fungi. See accompanying commentary: http://dx.doi.org/10.1002/eji.200737804
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Cites
A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17
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IL-23 drives a pathogenic T cell population that induces autoimmune inflammation
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Transforming growth factor-β induces development of the TH17 lineage
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Self-citationIdo expression by dendritic cells: tolerance and tryptophan catabolism
Mellor, A. L., & Munn, D. H. (2004) · Nature Reviews Immunology · doi:10.1038/nri1457 · Cited by 2,341
Surface phenotype and antigenic specificity of human interleukin 17–producing T helper memory cells
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Requirement of Interleukin‐17A for Systemic Anti– Candida albicans Host Defense in Mice
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Cited by
Romani, L. (2011) · Nature Reviews Immunology · doi:10.1038/nri2939 · Cited by 1,793
Self-citationConti, H. R., Shen, F., Nayyar, N., Stocum, E., Sun, J. N., Lindemann, M. J., Ho, A. W., Hai, J. H., Yu, J. J., Jung, J. W., et al. (2009) · Journal of Experimental Medicine · doi:10.1084/jem.20081463 · Cited by 1,024
An integrated model of the recognition of Candida albicans by the innate immune system
Netea, M. G., Brown, G. D., Kullberg, B. J., & Gow, N. A. R. (2008) · Nature Reviews Microbiology · doi:10.1038/nrmicro1815 · Cited by 946
Interleukin-17 and its target genes: mechanisms of interleukin-17 function in disease
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Emerging opportunistic yeast infections
Miceli, M. H., Díaz, J. A., & Lee, S. A. (2011) · The Lancet Infectious Diseases · doi:10.1016/s1473-3099(10)70218-8 · Cited by 811
Metadata
- Authors
- Zelante, T., De Luca, A., Bonifazi, P., Montagnoli, C., Bozza, S., Moretti, S., Belladonna, M. L., Vacca, C., Conte, C., Mosci, P., Bistoni, F., Puccetti, P., Kastelein, R. A., Kopf, M., & Romani, L.
- Venue
- European Journal of Immunology
- Publisher
- Wiley
- Published
- 2007-09-26
- Volume
- 37
- Issue
- 10
- Pages
- 2695-2706
- ISSN
- 0014-2980 (ISSN-L)
- 1521-4141
- OpenAlex
- W2094786750
- Cited by
- 555
- References
- 11
- FWCI
- 20.29
- Type
- journal article
- Language
- en
- Open access
- closed
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