The DOI matches its Crossref record; 161 of the 161 references it cites were found in a registry or an index.
Basic biology and role of interleukin‐17 in immunity and inflammation
Open accessAbstract
Interleukin‐17 (also known as interleukin‐17A) is a key cytokine that links T‐cell activation to neutrophil mobilization and activation. As such, interleukin‐17 can mediate protective innate immunity to pathogens or contribute to the pathogenesis of inflammatory diseases, such as psoriasis and rheumatoid arthritis. This review summarizes the basic biology of interleukin‐17 and discusses its emerging role in periodontal disease. The current burden of evidence from human and animal model studies suggests that the net effect of interleukin‐17 signaling promotes disease development. In addition to promoting neutrophilic inflammation, interleukin‐17 has potent pro‐osteoclastogenic effects that are likely to contribute to the pathogenesis of periodontitis, rheumatoid arthritis and other diseases involving bone immunopathology. Systemic treatments with anti‐interleukin‐17 biologics have shown promising results in clinical trials for psoriasis and rheumatoid arthritis; however, their impact on the highly prevalent periodontal disease has not been investigated or reported. Future clinical trials, preferably using locally administered interleukin‐17 blockers, are required to implicate conclusivelyinterleukin‐17 in periodontitis and, more importantly, to establish an effective adjunctive treatment for this oral inflammatory disease.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
1 retracted
Doreau, A., Belot, A., Bastid, J., Riche, B., Trescol-Biemont, M.-C., Ranchin, B., Fabien, N., Cochat, P., Pouteil-Noble, C., Trolliet, P., et al. (2009) · Nature Immunology · doi:10.1038/ni.1741 · Cited by 452
RetractedMosmann, T. R., Cherwinski, H., Bond, M. W., Giedlin, M. A., & Coffman, R. L. (1986) · The Journal of Immunology · doi:10.4049/jimmunol.136.7.2348 · Cited by 7,506
Mizgerd, J. P., Kubo, H., Kutkoski, G. J., Bhagwan, S. D., Scharffetter-Kochanek, K., Beaudet, A. L., & Doerschuk, C. M. (1997) · The Journal of Experimental Medicine · doi:10.1084/jem.186.8.1357 · Cited by 7,306
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
Osteoclast differentiation and activation
Boyle, W. J., Simonet, W. S., & Lacey, D. L. (2003) · Nature · doi:10.1038/nature01658 · Cited by 6,670 · cited 1×
“A persisting inflammatory environment can ultimately disrupt bone homeostasis, which depends on a triad of proteins within the tumor necrosis factor/ tumor necrosis factor-receptor family, consisting of RANKL, its functional receptor (RANK) and its decoy receptor (osteoprotegerin) (17).”
BackgroundNeutrophil recruitment and function in health and inflammation
Kolaczkowska, E., & Kubes, P. (2013) · Nature Reviews Immunology · doi:10.1038/nri3399 · Cited by 5,472
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
Harrington, L. E., Hatton, R. D., Mangan, P. R., Turner, H., Murphy, T. L., Murphy, K. M., & Weaver, C. T. (2005) · Nature Immunology · doi:10.1038/ni1254 · Cited by 4,742
A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17
Park, H., Li, Z., Yang, X. O., Chang, S. H., Nurieva, R., Wang, Y.-H., Wang, Y., Hood, L., Zhu, Z., Tian, Q., et al. (2005) · Nature Immunology · doi:10.1038/ni1261 · Cited by 4,265
Complement: a key system for immune surveillance and homeostasis
Ricklin, D., Hajishengallis, G., Yang, K., & Lambris, J. D. (2010) · Nature Immunology · doi:10.1038/ni.1923 · Cited by 3,654 · cited 1×
“Although normally tightly regulated (128), the complement system may become deregulated in a local niche, such as the gingival crevice, owing to a constant influx of microbial inflammatory molecules and the presence of periodontal bacteria that can subvert complement function (60, 64, 155).”
BackgroundSelf-citation
Cited by
Neutrophil: A Cell with Many Roles in Inflammation or Several Cell Types?
Rosales, C. (2018) · Frontiers in Physiology · doi:10.3389/fphys.2018.00113 · Cited by 1,334
Molecular aspects of the pathogenesis of periodontitis
Meyle, J., & Chapple, I. (2015) · Periodontology 2000 · doi:10.1111/prd.12104 · Cited by 705
Furue, M. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21155382 · Cited by 419
Dutzan, N., Kajikawa, T., Abusleme, L., Greenwell-Wild, T., Zuazo, C. E., Ikeuchi, T., Brenchley, L., Abe, T., Hurabielle, C., Martin, D., et al. (2018) · Science Translational Medicine · doi:10.1126/scitranslmed.aat0797 · Cited by 382
“In our current work, we focused on the TH17 cell subset, which is not only pivotal for oral antifungal immunity (11, 25) but also has been documented to expand in the oral inflammatory disease, periodontitis (6, 28, 29).”
Self-citationHost defense against oral microbiota by bone-damaging T cells
Tsukasaki, M., Komatsu, N., Nagashima, K., Nitta, T., Pluemsakunthai, W., Shukunami, C., Iwakura, Y., Nakashima, T., Okamoto, K., & Takayanagi, H. (2018) · Nature Communications · doi:10.1038/s41467-018-03147-6 · Cited by 322
Metadata
- Authors
- Zenobia, C., & Hajishengallis, G.
- Venue
- Periodontology 2000
- Publisher
- Wiley
- Published
- 2015-08-07
- Volume
- 69
- Issue
- 1
- Pages
- 142-159
- ISSN
- 0906-6713 (ISSN-L)
- 1600-0757
- OpenAlex
- W2143100947
- Cited by
- 470
- References
- 161
- FWCI
- 19.87
- Type
- journal article
- Language
- en
- Open access
- bronze
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Basic biology and role of interleukin‐17 in immunity and inflammation. https://app.cochat.ai/papers/10.1111/prd.12083
- The paper
- Zenobia, C., & Hajishengallis, G. (2015). Basic biology and role of interleukin‐17 in immunity and inflammation. Periodontology 2000. https://doi.org/10.1111/prd.12083
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
