The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.
IL-23 and Th17 Cells Enhance Th2-Cell–mediated Eosinophilic Airway Inflammation in Mice
Abstract
RATIONALE: The IL-23-IL-17A-producing CD4(+) T-cell (Th17 cell) axis plays an important role in the development of chronic inflammatory diseases, including autoimmune diseases. However, the role of the IL-23-Th17 cell axis in the regulation of allergic airway inflammation is still largely unknown. OBJECTIVES: To determine the role of IL-23 and Th17 cells in allergic airway inflammation. METHODS: We examined the effect of anti-IL-23 antibody on antigen-induced airway inflammation. We also investigated the effect of enforced expression of IL-23 on allergic airway inflammation by generating lung-specific IL-23 transgenic mice. Moreover, we examined the effect of adoptive transfer of antigen-specific Th17 cells on allergic airway inflammation. MEASUREMENTS AND MAIN RESULTS: IL-23 mRNA was expressed in the lung of sensitized mice upon antigen inhalation, and the neutralization of IL-23 decreased antigen-induced eosinophil recruitment and Th2 cytokine production in the airways. The enforced expression of IL-23 in the airways significantly enhanced antigen-induced eosinophil and neutrophil recruitment into the airways; Th2 cytokine, IL-17A, and tumor necrosis factor (TNF)-alpha production in the airways; goblet cell hyperplasia; and airway hyperresponsiveness. Moreover, IL-23-mediated enhancement of antigen-induced Th2 cytokine production and eosinophil recruitment in the airways was still observed in the mice lacking IL-17A. Furthermore, although adoptive transfer of antigen-specific Th17 cells alone induced neutrophil but not eosinophil recruitment into the airways upon antigen inhalation, cotransfer of Th17 cells with Th2 cells significantly enhanced antigen-induced Th2-cell-mediated eosinophil recruitment into the airways and airway hyperresponsiveness. CONCLUSIONS: IL-23 and Th17 cells not only induce Th17-cell-mediated neutrophilic airway inflammation but also up-regulate Th2-cell-mediated eosinophilic airway inflammation.
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Citations
Cites
IL-23 drives a pathogenic T cell population that induces autoimmune inflammation
Langrish, C. L., Chen, Y., Blumenschein, W. M., Mattson, J., Basham, B., Sedgwick, J. D., McClanahan, T., Kastelein, R. A., & Cua, D. J. (2005) · The Journal of Experimental Medicine · doi:10.1084/jem.20041257 · Cited by 4,099
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Divergent Pro- and Antiinflammatory Roles for IL-23 and IL-12 in Joint Autoimmune Inflammation
Murphy, C. A., Langrish, C. L., Chen, Y., Blumenschein, W., McClanahan, T., Kastelein, R. A., Sedgwick, J. D., & Cua, D. J. (2003) · The Journal of Experimental Medicine · doi:10.1084/jem.20030896 · Cited by 1,669
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Th17: An Effector CD4 T Cell Lineage with Regulatory T Cell Ties
Weaver, C. T., Harrington, L. E., Mangan, P. R., Gavrieli, M., & Murphy, K. M. (2006) · Immunity · doi:10.1016/j.immuni.2006.06.002 · Cited by 1,422
Regulation of inflammatory responses by IL-17F
Yang, X. O., Chang, S. H., Park, H., Nurieva, R., Shah, B., Acero, L., Wang, Y.-H., Schluns, K. S., Broaddus, R. R., Zhu, Z., et al. (2008) · The Journal of Experimental Medicine · doi:10.1084/jem.20071978 · Cited by 739
Cited by
Lambrecht, B. N., & Hammad, H. (2015) · Nature Immunology · doi:10.1038/ni.3049 · Cited by 1,673
Cao, P.-P., Li, H.-B., Wang, B.-F., Wang, S.-B., You, X.-J., Cui, Y.-H., Wang, D.-Y., Desrosiers, M., & Liu, Z. (2009) · Journal of Allergy and Clinical Immunology · doi:10.1016/j.jaci.2009.05.017 · Cited by 616
Arnold, I. C., Dehzad, N., Reuter, S., Martin, H., Becher, B., Taube, C., & Müller, A. (2011) · Journal of Clinical Investigation · doi:10.1172/jci45041 · Cited by 462
Lajoie, S., Lewkowich, I. P., Suzuki, Y., Clark, J. R., Sproles, A. A., Dienger, K., Budelsky, A. L., & Wills-Karp, M. (2010) · Nature Immunology · doi:10.1038/ni.1926 · Cited by 329
Modified Foxp3 mRNA protects against asthma through an IL-10-dependent mechanism
Mays, L. E., Ammon-Treiber, S., Mothes, B., Alkhaled, M., Rottenberger, J., Müller-Hermelink, E. S., Grimm, M., Mezger, M., Beer-Hammer, S., von Stebut, E., et al. (2013) · Journal of Clinical Investigation · doi:10.1172/jci65351 · Cited by 113
Metadata
- Authors
- Wakashin, H., Hirose, K., Maezawa, Y., Kagami, S.-I., Suto, A., Watanabe, N., Saito, Y., Hatano, M., Tokuhisa, T., Iwakura, Y., Puccetti, P., Iwamoto, I., & Nakajima, H.
- Venue
- American Journal of Respiratory and Critical Care Medicine
- Publisher
- Oxford University Press (OUP)
- Published
- 2008-11-15
- Volume
- 178
- Issue
- 10
- Pages
- 1023-1032
- ISSN
- 1073-449X (ISSN-L)
- 1535-4970
- OpenAlex
- W2139775496
- Cited by
- 437
- References
- 6
- FWCI
- 20.11
- Type
- journal article
- Language
- en
- Open access
- closed
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- The paper
- Wakashin, H., Hirose, K., Maezawa, Y., Kagami, S.-I., Suto, A., Watanabe, N., Saito, Y., Hatano, M., Tokuhisa, T., Iwakura, Y., Puccetti, P., Iwamoto, I., & Nakajima, H. (2008). IL-23 and Th17 Cells Enhance Th2-Cell–mediated Eosinophilic Airway Inflammation in Mice. American Journal of Respiratory and Critical Care Medicine. https://doi.org/10.1164/rccm.200801-086oc
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