ArticleScience translational medicine2014
Defective neutrophil recruitment in leukocyte adhesion deficiency type I disease causes local IL-17-driven inflammatory bone loss.
Article in Science translational medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 200 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
200 citing papers in PubMed, 2 syntheses or guidelines pooled it, 294 citations in OpenAlex.
- Association of neutrophil to lymphocyte ratio with bone mineral density in post-menopausal women: a systematic review and meta-analysis.BMC women's health · 2024Pooled it
- Polymorphisms in interleukins 17A and 17F genes and periodontitis: results from a meta-analysis.Molecular biology reports · 2017Pooled it
- Clinical and laboratory findings in patients with leukocyte adhesion deficiency type I: A multicenter study in Turkey.Clinical and experimental immunology · 2021Trial
- A dysbiotic microbiome triggers TScience translational medicine · 2018Trial
- Mechanistic Characterization of Biologically Inspired Oral Neutrophil Isolation for AI-Assisted Oral Inflammatory Load Assessment.Biomimetics (Basel, Switzerland) · 2026Article
- Clinical considerations for immune dysregulation and immunodeficiency in Down syndrome.Journal of human immunity · 2026Review
- TAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- IL-17 Receptor inhibition with brodalumab limits experimental periodontitis.Journal of translational medicine · 2026Article
- IL-22 synergizes with IL-17 to promote mucosal inflammation and bone loss.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Integrin Signaling Imbalance in Periodontitis: A Stage-Dependent Link Between Inflammation, Bone Resorption and Regenerative Failure.Biomolecules · 2026Review
- Review
- International clinical consensus on leukocyte adhesion deficiency-I: Modified Delphi analysis.The journal of allergy and clinical immunology. Global · 2026Article
- Tissue-specific adaptation of human T cells is preserved during tissue inflammation.bioRxiv : the preprint server for biology · 2026Article
- Maternal antibodies regulate the establishment of murine oral and salivary mucosal immunity.Nature communications · 2026Article
- Histological analysis of periodontal tissues in patients with autoimmune diseases: a comparative cross-sectional study of inflammatory cell infiltration and epithelial barrier function.BMC oral health · 2026Article
- Mucosal Inflammation Shapes Human Neutrophil States in Tissue and Circulation.bioRxiv : the preprint server for biology · 2026Article
- Cxcr2 is Required for Osteoclast Regulation, Bone Structure, and Hematological Response During Bone (Re)modeling.Calcified tissue international · 2026Article
- Bacteria-induced immunity: from homeostasis to immune subversion in periodontitis.Einstein (Sao Paulo, Brazil) · 2026Review
- The cross-talk between T and B lymphocytes and the oral microbiome in health and disease: a narrative review.Frontiers in immunology · 2026Review
- T-cell senescence and immunosenescence in chronic oral mucosal inflammatory diseases: mechanisms and therapeutic implications.Journal of oral microbiology · 2026Review
140 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
15 authors at 1 institution in 1 country.
Funding
Abstract
Leukocyte adhesion deficiency type I (LAD-I), a disease syndrome associated with frequent microbial infections, is caused by mutations on the CD18 subunit of β₂ integrins. LAD-I is invariably associated with severe periodontal bone loss, which historically has been attributed to the lack of neutrophil surveillance of the periodontal infection. We provide an alternative mechanism by showing that the cytokine interleukin-17 (IL-17) plays a major role in the oral pathology of LAD-I. Defective neutrophil recruitment in LAD-I patients or in LFA-1 (CD11a/CD18)-deficient mice--which exhibit the LAD-I periodontal phenotype--was associated with excessive production of predominantly T cell-derived IL-17 in the periodontal tissue, although innate lymphoid cells also contributed to pathological IL-17 elevation in the LFA-1-deficient mice. Local treatment with antibodies to IL-17 or IL-23 in LFA-1-deficient mice not only blocked inflammatory periodontal bone loss but also caused a reduction in the total bacterial burden, suggesting that the IL-17-driven pathogenesis of LAD-I periodontitis leads to dysbiosis. Therefore, our findings support an IL-17-targeted therapy for periodontitis in LAD-I patients.
Indexed as
Identifiers
What OpenQuestion holds
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.