The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.
An essential role for IL-17 in preventing pathogen-initiated bone destruction: recruitment of neutrophils to inflamed bone requires IL-17 receptor–dependent signals
Open accessAbstract
IL-17 and its receptor are founding members of a novel family of inflammatory cytokines. IL-17 plays a pathogenic role in rheumatoid arthritis (RA)–associated bone destruction. However, IL-17 is also an important regulator of host defense through granulopoiesis and neutrophil trafficking. Therefore, the role of IL-17 in pathogen-initiated bone loss was not obvious. The most common form of infection-induced bone destruction occurs in periodontal disease (PD). In addition to causing significant morbidity, PD is a risk factor for atherosclerotic heart disease and chronic obstructive pulmonary disease (COPD). Similar to RA, bone destruction in PD is caused by the immune response. However, neutrophils provide critical antimicrobial defense against periodontal organisms. Since IL-17 is bone destructive in RA but a key regulator of neutrophils, we examined its role in inflammatory bone loss induced by the oral pathogen Porphyromonas gingivalis in IL-17RA–deficient mice. These mice showed enhanced periodontal bone destruction, suggesting a bone-protective role for IL-17, reminiscent of a neutrophil deficiency. Although IL-17RA–deficient neutrophils functioned normally ex vivo, IL-17RA knock-out (IL-17RAKO) mice exhibited reduced serum chemokine levels and concomitantly reduced neutrophil migration to bone. Consistently, CXCR2KO mice were highly susceptible to alveolar bone loss; interestingly, these mice also suggested a role for chemokines in maintaining normal bone homeostasis. These results indicate a nonredundant role for IL-17 in mediating host defense via neutrophil mobilization.
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Cites
IL-23 drives a pathogenic T cell population that induces autoimmune inflammation
Langrish, C. L., Chen, Y., Blumenschein, W. M., Mattson, J., Basham, B., Sedgwick, J. D., McClanahan, T., Kastelein, R. A., & Cua, D. J. (2005) · The Journal of Experimental Medicine · doi:10.1084/jem.20041257 · Cited by 4,099
Kong, Y.-Y., Feige, U., Sarosi, I., Bolon, B., Tafuri, A., Morony, S., Capparelli, C., Li, J., Elliott, R., McCabe, S., et al. (1999) · Nature · doi:10.1038/46303 · Cited by 1,856
Sato, K., Suematsu, A., Okamoto, K., Yamaguchi, A., Morishita, Y., Kadono, Y., Tanaka, S., Kodama, T., Akira, S., Iwakura, Y., et al. (2006) · The Journal of Experimental Medicine · doi:10.1084/jem.20061775 · Cited by 1,554
T cell interleukin-17 induces stromal cells to produce proinflammatory and hematopoietic cytokines
Fossiez, F., Djossou, O., Chomarat, P., Flores-Romo, L., Ait-Yahia, S., Maat, C., Pin, J. J., Garrone, P., Garcia, E., Saeland, S., et al. (1996) · The Journal of Experimental Medicine · doi:10.1084/jem.183.6.2593 · Cited by 1,526
Th17: An Effector CD4 T Cell Lineage with Regulatory T Cell Ties
Weaver, C. T., Harrington, L. E., Mangan, P. R., Gavrieli, M., & Murphy, K. M. (2006) · Immunity · doi:10.1016/j.immuni.2006.06.002 · Cited by 1,422
Requirement of Interleukin‐17A for Systemic Anti– Candida albicans Host Defense in Mice
Huang, W., Na, L., Fidel, P. L., & Schwarzenberger, P. (2004) · The Journal of Infectious Diseases · doi:10.1086/422329 · Cited by 859
Hymowitz, S. G., Filvaroff, E. H., Yin, J., Lee, J., Cai, L., Risser, P., Maruoka, M., Mao, W., Foster, J., Kelley, R. F., et al. (2001) · The EMBO Journal · doi:10.1093/emboj/20.19.5332 · Cited by 548
Ruddy, M. J., Wong, G. C., Liu, X. K., Yamamoto, H., Kasayama, S., Kirkwood, K. L., & Gaffen, S. L. (2004) · Journal of Biological Chemistry · doi:10.1074/jbc.m308809200 · Cited by 364
Self-citationSchwandner, R., Yamaguchi, K., & Cao, Z. (2000) · The Journal of Experimental Medicine · doi:10.1084/jem.191.7.1233 · Cited by 349
Shen, F., Ruddy, M. J., Plamondon, P., & Gaffen, S. L. (2004) · Journal of Leukocyte Biology · doi:10.1189/jlb.0904490 · Cited by 268
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Korn, T., Bettelli, E., Oukka, M., & Kuchroo, V. K. (2009) · Annual Review of Immunology · doi:10.1146/annurev.immunol.021908.132710 · Cited by 4,873
The IL-17 Family of Cytokines in Health and Disease
McGeachy, M. J., Cua, D. J., & Gaffen, S. L. (2019) · Immunity · doi:10.1016/j.immuni.2019.03.021 · Cited by 1,443
Self-citationConti, H. R., Shen, F., Nayyar, N., Stocum, E., Sun, J. N., Lindemann, M. J., Ho, A. W., Hai, J. H., Yu, J. J., Jung, J. W., et al. (2009) · Journal of Experimental Medicine · doi:10.1084/jem.20081463 · Cited by 1,024
Interleukin-17 and its target genes: mechanisms of interleukin-17 function in disease
Onishi, R. M., & Gaffen, S. L. (2010) · Immunology · doi:10.1111/j.1365-2567.2009.03240.x · Cited by 894
Self-citationGarlet, G. P. (2010) · Journal of Dental Research · doi:10.1177/0022034510376402 · Cited by 720
Metadata
- Authors
- Yu, J. J., Ruddy, M. J., Wong, G. C., Sfintescu, C., Baker, P. J., Smith, J. B., Evans, R. T., & Gaffen, S. L.
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2007-01-03
- Volume
- 109
- Issue
- 9
- Pages
- 3794-3802
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- OpenAlex
- W2042881479
- Cited by
- 372
- References
- 11
- FWCI
- 26.47
- Type
- journal article
- Language
- en
- Open access
- bronze
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- CoChat. (2026). Citation check: An essential role for IL-17 in preventing pathogen-initiated bone destruction: recruitment of neutrophils to inflamed bone requires IL-17 receptor–dependent signals. https://app.cochat.ai/papers/10.1182/blood-2005-09-010116
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- Yu, J. J., Ruddy, M. J., Wong, G. C., Sfintescu, C., Baker, P. J., Smith, J. B., Evans, R. T., & Gaffen, S. L. (2007). An essential role for IL-17 in preventing pathogen-initiated bone destruction: recruitment of neutrophils to inflamed bone requires IL-17 receptor–dependent signals. Blood. https://doi.org/10.1182/blood-2005-09-010116
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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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