The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
Innate lymphoid cells responding to IL-33 mediate airway hyperreactivity independently of adaptive immunity
Open accessAbstract
Background Asthma has been considered an immunological disease mediated by Th2 cells and adaptive immunity. However, clinical and experimental observations suggest that additional pathways may regulate asthma, particularly in non-allergic forms of asthma, such as asthma associated with air pollution, stress, obesity and infection. Objectives Our goal was to understand Th2 cell-independent conditions which might lead to airway hyperreactivity (AHR), a cardinal feature of asthma. Methods We examined a mouse model of experimental asthma, in which AHR was induced with glycolipid antigens, which activate natural killer T (NKT) cells. Results In this model, AHR developed rapidly when mice were treated with NKT cell-activating glycolipid antigens, even in the absence of conventional CD4+ T cells. The activated NKT cells directly induced alveolar macrophages to produce IL-33, which in turn activated NKT cells as well as natural helper cells, a newly described non-T, non-B, innate lymphoid cell type, to increase production of IL-13. Surprisingly, this glycolipid-induced AHR pathway required not only IL-13, but also IL-33 and its receptor, ST2, since it was blocked by an anti-ST2 mAb, and was greatly reduced in ST2−/− mice. When adoptively transferred into IL-13−/− mice, both wildtype natural helper cells and NKT cells were sufficient for the development of glycolipid induced AHR. Conclusion Since plant pollens, house dust and some bacteria contain glycolipids that can directly activate NKT cells, these studies suggest that AHR and asthma can fully develop, or be greatly enhanced, through innate immune mechanisms, involving IL-33, natural helper cells and NKT cells.
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Mjösberg, J. M., Trifari, S., Crellin, N. K., Peters, C. P., van Drunen, C. M., Piet, B., Fokkens, W. J., Cupedo, T., & Spits, H. (2011) · Nature Immunology · doi:10.1038/ni.2104 · Cited by 1,166
Carriere, V., Roussel, L., Ortega, N., Lacorre, D.-A., Americh, L., Aguilar, L., Bouche, G., & Girard, J.-P. (2007) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0606854104 · Cited by 966
Increased expression of IL-33 in severe asthma: evidence of expression by airway smooth muscle cells
Préfontaine, D., Lajoie-Kadoch, S., Foley, S., Audusseau, S., Olivenstein, R., Halayko, A. J., Lemière, C., Martin, J. G., & Hamid, Q. (2009) · The Journal of Immunology · doi:10.4049/jimmunol.0802387 · Cited by 538
Kim, E. Y., Battaile, J. T., Patel, A. C., You, Y., Agapov, E., Grayson, M. H., Benoit, L. A., Byers, D. E., Alevy, Y., Tucker, J., et al. (2008) · Nature Medicine · doi:10.1038/nm1770 · Cited by 523
Lung interstitial macrophages alter dendritic cell functions to prevent airway allergy in mice
Bedoret, D., Wallemacq, H., Marichal, T., Desmet, C., Quesada Calvo, F., Henry, E., Closset, R., Dewals, B., Thielen, C., Gustin, P., et al. (2009) · Journal of Clinical Investigation · doi:10.1172/jci39717 · Cited by 399
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The family of the interleukin‐1 receptors
Boraschi, D., Italiani, P., Weil, S., & Martin, M. U. (2018) · Immunological Reviews · doi:10.1111/imr.12606 · Cited by 389
IL-33 promotes airway remodeling in pediatric patients with severe steroid-resistant asthma
Saglani, S., Lui, S., Ullmann, N., Campbell, G. A., Sherburn, R. T., Mathie, S. A., Denney, L., Bossley, C. J., Oates, T., Walker, S. A., et al. (2013) · Journal of Allergy and Clinical Immunology · doi:10.1016/j.jaci.2013.04.012 · Cited by 258
McSorley, H. J., Blair, N. F., Smith, K. A., McKenzie, A. N. J., & Maizels, R. M. (2014) · Mucosal Immunology · doi:10.1038/mi.2013.123 · Cited by 163
Self-citationDietary Fiber-Induced Microbial Short Chain Fatty Acids Suppress ILC2-Dependent Airway Inflammation
Lewis, G., Wang, B., Shafiei Jahani, P., Hurrell, B. P., Banie, H., Aleman Muench, G. R., Maazi, H., Helou, D. G., Howard, E., Galle-Treger, L., et al. (2019) · Frontiers in Immunology · doi:10.3389/fimmu.2019.02051 · Cited by 163
Metadata
- Authors
- Kim, H. Y., Chang, Y.-J., Subramanian, S., Lee, H.-H., Albacker, L. A., Matangkasombut, P., Savage, P. B., McKenzie, A. N. J., Smith, D. E., Rottman, J. B., DeKruyff, R. H., & Umetsu, D. T.
- Venue
- Journal of Allergy and Clinical Immunology
- Publisher
- Elsevier BV
- Published
- 2012-01
- Volume
- 129
- Issue
- 1
- Pages
- 216-227.e6
- ISSN
- 0091-6749 (ISSN-L)
- OpenAlex
- W2027462139
- Cited by
- 316
- References
- 5
- FWCI
- 13.01
- Type
- journal article
- Language
- en
- Open access
- green
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- Kim, H. Y., Chang, Y.-J., Subramanian, S., Lee, H.-H., Albacker, L. A., Matangkasombut, P., Savage, P. B., McKenzie, A. N. J., Smith, D. E., Rottman, J. B., DeKruyff, R. H., & Umetsu, D. T. (2012). Innate lymphoid cells responding to IL-33 mediate airway hyperreactivity independently of adaptive immunity. Journal of Allergy and Clinical Immunology. https://doi.org/10.1016/j.jaci.2011.10.036
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