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Alternative splicing of interleukin-33 and type 2 inflammation in asthma

Gordon, Erin D., Simpson, Laura J., Rios, Cydney L., Ringel, Lando, Lachowicz-Scroggins, Marrah E., Peters, Michael C., Wesolowska-Andersen, Agata, Gonzalez, Jeanmarie R., MacLeod, Hannah J., Christian, Laura S., Yuan, Shaopeng, Barry, Liam, Woodruff, Prescott G., Ansel, K. Mark, Nocka, Karl, Seibold, Max A., Fahy, John V.·2016·Proceedings of the National Academy of Sciences
DOI 10.1073/pnas.1601914113
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Abstract

Significance: Type 2 inflammation occurs in a large subgroup of asthmatics and is the target of multiple novel therapies for asthma; however, the mechanisms that drive type 2 inflammation in chronic asthma are poorly understood. In this study, we identify a previously unidentified mechanism of IL-33 activity involving alternative RNA transcript splicing and provide evidence that mast cells and basophils are major cellular targets of IL-33 activity driving type 2 cytokine production in stable asthma. These data advance our understanding of the mechanisms of type 2-high asthma and guide the selection of asthmatics likely to benefit from IL-33 inhibitor therapies.

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Research works printed but not linked: 42

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Metadata

Authors
Gordon, E. D., Simpson, L. J., Rios, C. L., Ringel, L., Lachowicz-Scroggins, M. E., Peters, M. C., Wesolowska-Andersen, A., Gonzalez, J. R., MacLeod, H. J., Christian, L. S., Yuan, S., Barry, L., Woodruff, P. G., Ansel, K. M., Nocka, K., Seibold, M. A., & Fahy, J. V.
Affiliations
  • Department of Pulmonary and Critical Care Medicine, University of California, San Francisco, CA 94143;
  • Department of Microbiology and Immunology, University of California San Francisco, CA 94143;
  • Center for Genes, Environment, and Health, National Jewish Health, Denver, CO 80206;
  • Cardiovascular Research Institute, University of California, San Francisco, CA 94143;
  • Immunoscience, Pfizer Worldwide Research and Development, Cambridge, MA 02139;
ORCID
Venue
Proceedings of the National Academy of Sciences
Publisher
National Academy of Sciences
Published
2016-07-18
Volume
113
Issue
31
Pages
8765-8770
ISSN
  • 0027-8424
  • 1091-6490
DOI
10.1073/pnas.1601914113
Cited by
153
References
5
Language
en
Licence
www.pnas.org/preview_site/misc/userlicense.xhtml (vor)
Funders
  • HHS | NIH | National Heart, Lung, and Blood Institute (5P01HL107202-02, 1K08HL114645-01A1)
  • Pfizer (none)

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CoChat. (2026). Citation check: Alternative splicing of interleukin-33 and type 2 inflammation in asthma. https://app.cochat.ai/papers/10.1073/pnas.1601914113
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Gordon, E. D., Simpson, L. J., Rios, C. L., Ringel, L., Lachowicz-Scroggins, M. E., Peters, M. C., Wesolowska-Andersen, A., Gonzalez, J. R., MacLeod, H. J., Christian, L. S., Yuan, S., Barry, L., Woodruff, P. G., Ansel, K. M., Nocka, K., Seibold, M. A., & Fahy, J. V. (2016). Alternative splicing of interleukin-33 and type 2 inflammation in asthma. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.1601914113