The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
Interleukin-17 is a negative regulator of established allergic asthma
Open accessAbstract
T helper (Th)17 cells producing interleukin (IL)-17 play a role in autoimmune and allergic inflammation. Here, we show that IL-23 induces IL-17 in the lung and IL-17 is required during antigen sensitization to develop allergic asthma, as shown in IL-17R–deficient mice. Since IL-17 expression increased further upon antigen challenge, we addressed its function in the effector phase. Most strikingly, neutralization of IL-17 augmented the allergic response in sensitized mice. Conversely, exogenous IL-17 reduced pulmonary eosinophil recruitment and bronchial hyperreactivity, demonstrating a novel regulatory role of IL-17. Mechanistically, IL-17 down modulated eosinophil-chemokine eotaxin (CCL11) and thymus- and activation-regulated chemokine/CCL17 (TARC) in lungs in vivo and ex vivo upon antigen restimulation. In vitro, IL-17 reduced TARC production in dendritic cells (DCs)—the major source of TARC—and antigen uptake by DCs and IL-5 and IL-13 production in regional lymph nodes. Furthermore, IL-17 is regulated in an IL-4–dependent manner since mice deficient for IL-4Rα signaling showed a marked increase in IL-17 concentration with inhibited eosinophil recruitment. Therefore, endogenous IL-17 is controlled by IL-4 and has a dual role. Although it is essential during antigen sensitization to establish allergic asthma, in sensitized mice IL-17 attenuates the allergic response by inhibiting DCs and chemokine synthesis.
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A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17
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Divergent Pro- and Antiinflammatory Roles for IL-23 and IL-12 in Joint Autoimmune Inflammation
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Requirement of Interleukin‐17A for Systemic Anti– Candida albicans Host Defense in Mice
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Cited by
Lambrecht, B. N., & Hammad, H. (2015) · Nature Immunology · doi:10.1038/ni.3049 · Cited by 1,673
Steinman, L. (2007) · Nature Medicine · doi:10.1038/nm1551 · Cited by 1,376
Functional Specialization of Interleukin-17 Family Members
Iwakura, Y., Ishigame, H., Saijo, S., & Nakae, S. (2011) · Immunity · doi:10.1016/j.immuni.2011.02.012 · Cited by 1,289
Impaired TH17 cell differentiation in subjects with autosomal dominant hyper-IgE syndrome
Milner, J. D., Brenchley, J. M., Laurence, A., Freeman, A. F., Hill, B. J., Elias, K. M., Kanno, Y., Spalding, C., Elloumi, H. Z., Paulson, M. L., et al. (2008) · Nature · doi:10.1038/nature06764 · Cited by 1,157
TH17 cells in development: an updated view of their molecular identity and genetic programming
Dong, C. (2008) · Nature reviews. Immunology · doi:10.1038/nri2295 · Cited by 1,064
Metadata
- Authors
- Schnyder-Candrian, S., Togbe, D., Couillin, I., Mercier, I., Brombacher, F., Quesniaux, V., Fossiez, F., Ryffel, B., & Schnyder, B.
- Venue
- The Journal of Experimental Medicine
- Publisher
- Rockefeller University Press
- Published
- 2006-11-13
- Volume
- 203
- Issue
- 12
- Pages
- 2715-2725
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- OpenAlex
- W2170644000
- Cited by
- 564
- References
- 7
- FWCI
- 30.97
- Type
- journal article
- Language
- en
- Open access
- bronze
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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