Interleukin‐11 and IL‐17 and the Pathogenesis of Periodontal Disease

Johnson, Roger B.; Wood, Neil; Serio, Francis G.

doi:10.1902/jop.2004.75.1.37

Cited by 168 publications

(177 citation statements)

References 53 publications

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“…In vitro studies have reported that treatment of healthy human periodontal ligament cells with lipopolysaccharide (LPS) from inflammatory pathogens involved in perio-http://bmbreports.org BMB reports dontal disease stimulates IL-6 release (56). Local expression of IL-6 at periodontic sites is higher than levels in similar sites in healthy controls (57,58). Surprisingly however, periodontal lesions induced by pulp exposure were larger in IL-6 null mice than wild type, but this model does not involve infection (59).…”

Section: Gp130 and Periodontal Diseasementioning

confidence: 84%

“…OSM has also been detected at high levels in periodontal endothelial and inflammatory cells (60), in gingival fluid (61) and in the circulation of patients with chronic periodontal disease (62), but is not observed in these locations in healthy subjects, suggesting that OSM may contribute to ongoing pathogenesis in this condition. In contrast, local expression of IL-11 is high in pockets of gingivitis (early stage periodontitis), but is low in established chronic periodontitis, suggesting a role for IL-11 in disease establishment only (58). No involvement of CT-1, CNTF or LIF in periodontal disease has been reported.…”

Section: Gp130 and Periodontal Diseasementioning

confidence: 98%

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GP130 cytokines and bone remodelling in health and disease

Sims¹,

Walsh²

2010

BMB Reports

108

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Gp130 cytokinesGlycoprotein 130 (gp130) is a receptor subunit capable of intracellular signalling that is required for the cellular action of a wide range of cytokines. The most well known of these are interleukin (IL-) 6 and IL-11, leukemia inhibitory factor (LIF), cardiotrophin-1 (CT-1), oncostatin M (OSM) and ciliary neurotrophic factor (CNTF). Every cytokine that binds to gp130 generates specific intracellular signalling events by forming specific receptor:ligand complexes, each with distinct components and/or architecture (Fig.

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Section: Gp130 and Periodontal Diseasementioning

confidence: 84%

Section: Gp130 and Periodontal Diseasementioning

confidence: 98%

GP130 cytokines and bone remodelling in health and disease

Sims¹,

Walsh²

2010

BMB Reports

108

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“…IL-11 induces bronchial inflammation (35,36), and it is induced by respiratory viral infections (37,38). Parallel increases in the IL-11 and IL-17 gene expression have been demonstrated in the animal model of rheumatoid arthritis (39), in inflammatory periodontal disease (40), and in the gastrointestinal mucosal Th17 cell inflammatory infiltrate associated with IL-11/STAT3 overexpression (29). The chromosomal region containing the IL-11 gene (19q13) has been associated with susceptibility to MS (41); however, its role in the development of the inflammatory response in MS has not been elucidated.…”

mentioning

confidence: 96%

IL-11 Induces Th17 Cell Responses in Patients with Early Relapsing-Remitting Multiple Sclerosis

Zhang

Tao

Chopra

et al. 2015

The Journal of Immunology

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Clinically isolated syndrome (CIS) suggestive of multiple sclerosis (MS) is the earliest clinically evident phase of the disease, which may provide valuable insight into the molecular mechanisms of the initiation of the autoimmune response in MS. Our results introduce IL-11 as a new cytokine that plays a role in the autoimmune response in the early phase of the disease. IL-11 is the highest upregulated cytokine in the sera and cerebrospinal fluid from CIS patients, which is also increased in patients with clinically definitive relapsing-remitting MS in comparison with healthy control subjects. Serum IL-11 levels are significantly increased during clinical exacerbations in comparison with remissions in the same patients. CD4+ cells represent a predominant cell source of IL-11 in the peripheral circulation, and the percentage of IL-11+CD4+ cells is significantly increased in CIS patients in comparison with healthy control subjects. Furthermore, we have identified IL-11 as a new Th17-promoting cytokine, because it induces a differentiation of naive CD4+ T cells into Th17 cells, as well as expansion of Th17 memory cells. Because the Th17 cytokines IL-17F, IL-21 and TNF-α, and TGF-β induce differentiation of naive cells in the IL-11–secreting CD4+ cells, we propose that cross-talk between IL-11+CD4+ and Th17 cells may play a role in the inflammatory response in relapsing-remitting MS.

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“…This cytokine is found at elevated levels in many inflammatory conditions in humans, particularly rheumatoid arthritis and lung airway infections (reviewed in Refs. 4 -7), but also Heliobacter pylori infection (8), multiple sclerosis (9), periodontal disease (10,11), and psoriasis (12). Mice deficient in the IL-17R also show an impaired ability to recover from Klebsiella pneumoniae infections (13).…”

mentioning

confidence: 99%

Crucial Role for Nuclear Factor of Activated T Cells in T Cell Receptor-mediated Regulation of Human Interleukin-17

Liu

Lin

Gaffen

2004

Journal of Biological Chemistry

152

127

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The biological activities of the inflammatory cytokine interleukin (IL)-17 have been widely studied. However, comparatively little is known about how IL-17 expression is controlled. Here, we examined the basis for transcriptional regulation of the human IL-17 gene. IL-17 secretion was induced in peripheral blood mononuclear cells following anti-CD3 cross-linking to activate the T cell receptor (TCR), and costimulatory signaling through CD28 strongly enhanced CD3-induced IL-17 production. To define cis-acting elements important for IL-17 gene regulation, we cloned 1.25 kb of genomic sequence upstream of the transcriptional start site. This putative promoter was active in Jurkat T cells following CD3 and CD28 cross-linking, and its activity was inhibited by cyclosporin A and MAPK inhibitors. The promoter was also active in Hut102 T cells, which we have shown to secrete IL-17 constitutively. Overexpression of nuclear factor of activated T cells (NFAT) or Ras enhanced IL-17 promoter activity, and studies in Jurkat lines deficient in specific TCR signaling pathways provided supporting evidence for a role for NFAT. To delineate the IL-17 minimal promoter, we created a series of 5 truncations and identified a region between ؊232 and ؊159 that was sufficient for inducible promoter activity. Interestingly, two NFAT sites were located within this region, which bound to NFATc1 and NFATc2 in nuclear extracts from Hut102 and Jurkat cells. Moreover, mutations of these sites dramatically reduced both specific DNA binding and reporter gene activity, and chromatin immunoprecipitation assays showed occupancy of NFAT at this region in vivo. Together, these data show that NFAT is the crucial sensor of TCR signaling in the IL-17 promoter.

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Interleukin‐11 and IL‐17 and the Pathogenesis of Periodontal Disease

Cited by 168 publications

References 53 publications

GP130 cytokines and bone remodelling in health and disease

GP130 cytokines and bone remodelling in health and disease

IL-11 Induces Th17 Cell Responses in Patients with Early Relapsing-Remitting Multiple Sclerosis

Crucial Role for Nuclear Factor of Activated T Cells in T Cell Receptor-mediated Regulation of Human Interleukin-17

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