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Basic biology and role of interleukin‐17 in immunity and inflammation

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Zenobia, Camille, Hajishengallis, George·2015·Periodontology 2000

DOI 10.1111/prd.12083

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Abstract

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.

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IL-17 and IL-11 GCF Levels in Aggressive and Chronic Periodontitis Patients: Relation to PCR Bacterial Detection
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Association between Polymorphisms in Interleukin-17A and -17F Genes and Chronic Periodontal Disease
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Expression and Function of the Homeostatic Molecule Del-1 in Endothelial Cells and the Periodontal Tissue
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“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).”
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Host 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

See all 470

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
DOI: 10.1111/prd.12083
OpenAlex: W2143100947
Cited by: 470
References: 162
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 ›

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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.

Basic biology and role of interleukin‐17 in immunity and inflammation

Abstract

Overview

Integrity signals

Verification

Claims the paper makes

Self-check

Citations

Cites

Cited by

Metadata

Record

About these checks

Data sources