The DOI matches its Crossref record; 31 of the 31 references it cites were found in a registry or an index.
Allergic Sensitization through the Airway Primes Th17-dependent Neutrophilia and Airway Hyperresponsiveness
Open accessAbstract
RATIONALE: In humans, immune responses to inhaled aeroallergens develop in the lung and draining lymph nodes. Many animal models of asthma bypass this route and instead use intraperitoneal injections of allergen using aluminum hydroxide as an adjuvant. OBJECTIVES: We investigated whether allergic sensitization through the airway elicits immune responses qualitatively different than those arising in the peritoneum. METHODS: Mice were sensitized to allergen through the airway using low-dose LPS as an adjuvant, or through the peritoneum using aluminum hydroxide as an adjuvant. After a single allergen challenge, ELISA and flow cytometry were used to measure cytokines and leukocyte subsets. Invasive measurements of airway resistance were used to measure allergen-induced airway hyperreactivity (AHR). MEASUREMENTS AND MAIN RESULTS: Sensitization through the peritoneum primed strong Th2 responses and eosinophilia, but not AHR, after a single allergen challenge. By contrast, allergic sensitization through the airway primed only modest Th2 responses, but strong Th17 responses. Th17 cells homed to the lung and released IL-17 into the airway on subsequent encounter with inhaled allergen. As a result, these mice developed IL-17-dependent airway neutrophilia and AHR. This AHR was neutrophil-dependent because it was abrogated in CXCR2-deficient mice and also in wild-type mice receiving a neutrophil-depleting antibody. Individually, neither IL-17 nor ongoing Th2 responses were sufficient to confer AHR, but together they acted synergistically to promote neutrophil recruitment, eosinophil recruitment and AHR. CONCLUSIONS: Allergic sensitization through the airway primes modest Th2 responses but strong Th17 responses that promote airway neutrophilia and acute AHR. These findings support a causal role for neutrophils in severe asthma.
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A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17
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Self-citationYe, P., Rodriguez, F. H., Kanaly, S., Stocking, K. L., Schurr, J., Schwarzenberger, P., Oliver, P., Huang, W., Zhang, P., Zhang, J., et al. (2001) · The Journal of Experimental Medicine · doi:10.1084/jem.194.4.519 · Cited by 1,521
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IL-17 is increased in asthmatic airways and induces human bronchial fibroblasts to produce cytokines
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Neutrophil Recruitment by Human IL-17 Via C-X-C Chemokine Release in the Airways
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Regulation of inflammatory responses by IL-17F
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Cited by
CD4 + T-cell subsets in inflammatory diseases: beyond the T h 1/T h 2 paradigm
Hirahara, K., & Nakayama, T. (2016) · International Immunology · doi:10.1093/intimm/dxw006 · Cited by 417
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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
Importance of Cytokines in Murine Allergic Airway Disease and Human Asthma
Finkelman, F. D., Hogan, S. P., Hershey, G. K. K., Rothenberg, M. E., & Wills-Karp, M. (2010) · The Journal of Immunology · doi:10.4049/jimmunol.0902185 · Cited by 293
Kitamura, H., Cambier, S., Somanath, S., Barker, T., Minagawa, S., Markovics, J., Goodsell, A., Publicover, J., Reichardt, L., Jablons, D., et al. (2011) · Journal of Clinical Investigation · doi:10.1172/jci45589 · Cited by 189
Metadata
- Authors
- Wilson, R. H., Whitehead, G. S., Nakano, H., Free, M. E., Kolls, J. K., & Cook, D. N.
- Venue
- American Journal of Respiratory and Critical Care Medicine
- Publisher
- Oxford University Press (OUP)
- Published
- 2009-10-15
- Volume
- 180
- Issue
- 8
- Pages
- 720-730
- ISSN
- 1073-449X (ISSN-L)
- 1535-4970
- OpenAlex
- W1972025293
- Cited by
- 403
- References
- 31
- FWCI
- 19.88
- Type
- journal article
- Language
- en
- Open access
- green
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- Wilson, R. H., Whitehead, G. S., Nakano, H., Free, M. E., Kolls, J. K., & Cook, D. N. (2009). Allergic Sensitization through the Airway Primes Th17-dependent Neutrophilia and Airway Hyperresponsiveness. American Journal of Respiratory and Critical Care Medicine. https://doi.org/10.1164/rccm.200904-0573oc
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