The DOI matches its Crossref record; 12 of the 12 references it cites were found in a registry or an index.
Pathological versus protective functions of IL-22 in airway inflammation are regulated by IL-17A
Open accessAbstract
IL-22 has both proinflammatory and tissue-protective properties depending on the context in which it is expressed. However, the factors that influence the functional outcomes of IL-22 expression remain poorly defined. We demonstrate that after administration of a high dose of bleomycin that induces acute tissue damage and airway inflammation and is lethal to wild-type (WT) mice, Th17 cell–derived IL-22 and IL-17A are expressed in the lung. Bleomycin-induced disease was ameliorated in Il22−/− mice or after anti–IL-22 monoclonal antibody (mAb) treatment of WT mice, indicating a proinflammatory/pathological role for IL-22 in airway inflammation. However, despite increased bleomycin-induced IL-22 production, Il17a−/− mice were protected from airway inflammation, suggesting that IL-17A may regulate the expression and/or proinflammatory properties of IL-22. Consistent with this, IL-17A inhibited IL-22 production by Th17 cells, and exogenous administration of IL-22 could only promote airway inflammation in vivo by acting in synergy with IL-17A. Anti–IL-22 mAb was delivered to Il17a−/− mice and was found to exacerbate bleomycin-induced airway inflammation, indicating that IL-22 is tissue protective in the absence of IL-17A. Finally, in an in vitro culture system, IL-22 administration protected airway epithelial cells from bleomycin-induced apoptosis, and this protection was reversed after coadministration of IL-17A. These data identify that IL-17A can regulate the expression, proinflammatory properties, and tissue-protective functions of IL-22, and indicate that the presence or absence of IL-17A governs the proinflammatory versus tissue-protective properties of IL-22 in a model of airway damage and inflammation.
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Cites
Bettelli, E., Carrier, Y., Gao, W., Korn, T., Strom, T. B., Oukka, M., Weiner, H. L., & Kuchroo, V. K. (2006) · Nature · doi:10.1038/nature04753 · Cited by 6,992
Transforming growth factor-β induces development of the TH17 lineage
Mangan, P. R., Harrington, L. E., O'Quinn, D. B., Helms, W. S., Bullard, D. C., Elson, C. O., Hatton, R. D., Wahl, S. M., Schoeb, T. R., & Weaver, C. T. (2006) · Nature · doi:10.1038/nature04754 · Cited by 3,087
Liang, S. C., Tan, X.-Y., Luxenberg, D. P., Karim, R., Dunussi-Joannopoulos, K., Collins, M., & Fouser, L. A. (2006) · The Journal of Experimental Medicine · doi:10.1084/jem.20061308 · Cited by 2,330
Self-citationStructure and signalling in the IL-17 receptor family
Gaffen, S. L. (2009) · Nature reviews. Immunology · doi:10.1038/nri2586 · Cited by 1,475
Production of interleukin 22 but not interleukin 17 by a subset of human skin-homing memory T cells
Duhen, T., Geiger, R., Jarrossay, D., Lanzavecchia, A., & Sallusto, F. (2009) · Nature Immunology · doi:10.1038/ni.1767 · Cited by 1,079 · cited 1×
“RT-PCR was performed subsets of gut-resident NK cells and skin-resident CD4+ T cells are reported to express IL-22 but do not coexpress IL-17A (Satoh-Takayama et al., 2008; Cella et al., 2009; Duhen et al., 2009; Trifari et al., 2009).”
BackgroundSTAT3 links IL-22 signaling in intestinal epithelial cells to mucosal wound healing
Pickert, G., Neufert, C., Leppkes, M., Zheng, Y., Wittkopf, N., Warntjen, M., Lehr, H.-A., Hirth, S., Weigmann, B., Wirtz, S., et al. (2009) · Journal of Experimental Medicine · doi:10.1084/jem.20082683 · Cited by 1,043
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IL-6 induces an anti-inflammatory response in the absence of SOCS3 in macrophages
Yasukawa, H., Ohishi, M., Mori, H., Murakami, M., Chinen, T., Aki, D., Hanada, T., Takeda, K., Akira, S., Hoshijima, M., et al. (2003) · Nature Immunology · doi:10.1038/ni938 · Cited by 771
A protective function for interleukin 17A in T cell–mediated intestinal inflammation
O'Connor Jr, W., Kamanaka, M., Booth, C. J., Town, T., Nakae, S., Iwakura, Y., Kolls, J. K., & Flavell, R. A. (2009) · Nature Immunology · doi:10.1038/ni.1736 · Cited by 756
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 2×
“It is possible that other Th17 cell–derived cytokines such as IL-17F or TNF- may play a significant role in this context, as well as other nonrelated inflammatory cytokines such as IFN-, all of which have been shown to contribute to airway inflammation in other model systems (Lukacs et al., 1995; Segel et al., 2003;…”
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Cited by
Interleukin-23-Independent IL-17 Production Regulates Intestinal Epithelial Permeability
Lee, J. S., Tato, C. M., Joyce-Shaikh, B., Gulen, M. F., Cayatte, C., Chen, Y., Blumenschein, W. M., Judo, M., Ayanoglu, G., McClanahan, T. K., et al. (2015) · Immunity · doi:10.1016/j.immuni.2015.09.003 · Cited by 760
Innate lymphoid cells sustain colon cancer through production of interleukin-22 in a mouse model
Kirchberger, S., Royston, D. J., Boulard, O., Thornton, E., Franchini, F., Szabady, R. L., Harrison, O., & Powrie, F. (2013) · Journal of Experimental Medicine · doi:10.1084/jem.20122308 · Cited by 529
Innate lymphoid cells in the initiation, regulation and resolution of inflammation
Sonnenberg, G. F., & Artis, D. (2015) · Nature Medicine · doi:10.1038/nm.3892 · Cited by 503
Self-citationA cellular and molecular view of T helper 17 cell plasticity in autoimmunity
Stadhouders, R., Lubberts, E., & Hendriks, R. W. (2018) · Journal of Autoimmunity · doi:10.1016/j.jaut.2017.12.007 · Cited by 282
The Th17 family: flexibility follows function
Basu, R., Hatton, R. D., & Weaver, C. T. (2013) · Immunological Reviews · doi:10.1111/imr.12035 · Cited by 229
Metadata
- Authors
- Sonnenberg, G. F., Nair, M. G., Kirn, T. J., Zaph, C., Fouser, L. A., & Artis, D.
- Venue
- Journal of Experimental Medicine
- Publisher
- Rockefeller University Press
- Published
- 2010-05-24
- Volume
- 207
- Issue
- 6
- Pages
- 1293-1305
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- OpenAlex
- W2098315859
- Cited by
- 380
- References
- 12
- FWCI
- 12.65
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Sonnenberg, G. F., Nair, M. G., Kirn, T. J., Zaph, C., Fouser, L. A., & Artis, D. (2010). Pathological versus protective functions of IL-22 in airway inflammation are regulated by IL-17A. Journal of Experimental Medicine. https://doi.org/10.1084/jem.20092054
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