ArticleBlood2007
An essential role for IL-17 in preventing pathogen-initiated bone destruction: recruitment of neutrophils to inflamed bone requires IL-17 receptor-dependent signals.
Article in Blood, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 162 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
162 citing papers in PubMed, 2 syntheses or guidelines pooled it, 370 citations in OpenAlex.
- Intraepithelial lymphocytes in human oral diseases.Frontiers in immunology · 2025Pooled it
- γδ T cells in oral diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Pooled it
- A thermosensitive hydrogel encapsulating 2-DG alleviates periodontitis by inhibiting glycolysis and effector response of Th17 cells.Frontiers in pharmacology · 2026Article
- B cell-intrinsic interleukin 17 receptor A signaling supports the establishment of chronic murine gammaherpesvirus 68 infection.Journal of virology · 2025Article
- The Role of IL-17 in Periodontitis and Its Systemic Connections.International journal of molecular sciences · 2025Review
- Synergizing adaptive immunity and regenerative signals to enhance osteochondral defects repair.Bioactive materials · 2025Article
- Immune response and cytokine pathways in psoriatic arthritis: A systematic review.Archives of rheumatology · 2025Review
- CRISPRJournal of oral microbiology · 2025Article
- Effect of Oral Pathogens Associated With Pulpitis and Apical Periodontitis on Odontogenic Mesenchymal Stem Cells.Stem cells international · 2025Review
- The dual role of IL-17 in periodontitis regulating immunity and bone homeostasis.Frontiers in immunology · 2025Review
- Molecular Mimicry Between Gut Microbiome and Rheumatoid Arthritis: Current Concepts.Medical sciences (Basel, Switzerland) · 2024Review
- Enthesitis on Chip - A Model for Studying Acute and Chronic Inflammation of the Enthesis and its Pharmacological Treatment.Advanced healthcare materials · 2024Article
- Therapeutic delivery of CCL2 modulates immune response and restores host-microbe homeostasis.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Therapeutic Effects of Hinokitiol through Regulating the SIRT1/NOX4 against Ligature-Induced Experimental Periodontitis.Antioxidants (Basel, Switzerland) · 2024Article
- Oral microbiota-host interaction: the chief culprit of alveolar bone resorption.Frontiers in immunology · 2024Review
- Cytokines in gingivitis and periodontitis: from pathogenesis to therapeutic targets.Frontiers in immunology · 2024Review
- Pharmacology and therapeutic potential of agarwood and agarwood tree leaves in periodontitis.Frontiers in pharmacology · 2024Review
- Preliminary Investigation and Therapeutic Efficacy Determination of a Novel Anti-IL-17A Antibody, Indikizumab.Biologics : targets & therapy · 2024Article
- Disruption of IL-17-mediated immunosurveillance in the respiratory mucosa results in invasiveFrontiers in immunology · 2024Article
- Chronological analysis of periodontal bone loss in experimental periodontitis in mice.Clinical and experimental dental research · 2023Article
102 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
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-17RA(KO)) mice exhibited reduced serum chemokine levels and concomitantly reduced neutrophil migration to bone. Consistently, CXCR2(KO) 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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.