Interleukin 34 expression is associated with synovitis severity in rheumatoid arthritis patients

Chemel, Marguerite; Goff, Benoît Le; Brion, Régis; Cozic, Céline; Berreur, Martine; Amiaud, Jérôme; Bougras, Gwenola; Touchais, S.; Blanchard, Frédéric; Heymann, Marie-Françoise; Berthelot, J. M.; Verrecchia, Franck; Heymann, Dominique

doi:10.1136/annrheumdis-2011-200096

Cited by 136 publications

(142 citation statements)

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“…The pro-inflammatory cytokines TNF-α and IL-1β regulate IL-34 expression in synovial and gingival fibroblasts by a mechanism involving NF-κB and MAPK 5,8) . Martinez 21) .…”

Section: Discussionmentioning

confidence: 99%

“…It is likely that IL-34 plays a role in inflammation, as it increases IL-6 and chemokine levels in human whole blood 11) . Interleukin-34 is also expressed in rheumatoid arthritis (RA) synovium, where it has been shown to be associated with severity of synovitis, and is elevated in serum and synovial fluid from RA patients 8) . Furthermore, IL-34 is produced by synovial and gingival fibroblasts in response to TNF-α and IL-1β through the NF-κB and c-Jun N-terminal kinase (JNK) pathways 5,8) .…”

Section: Introductionmentioning

confidence: 99%

“…Interleukin-34 is also expressed in rheumatoid arthritis (RA) synovium, where it has been shown to be associated with severity of synovitis, and is elevated in serum and synovial fluid from RA patients 8) . Furthermore, IL-34 is produced by synovial and gingival fibroblasts in response to TNF-α and IL-1β through the NF-κB and c-Jun N-terminal kinase (JNK) pathways 5,8) . Expression of IL-34 is also up-regulated in intestine in patients with inflammatory bowel disease (IBD) 31) and in inflamed salivary glands in patients with Sjögren's syndrome 10) .…”

Section: Introductionmentioning

confidence: 99%

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Interleukin-34 Levels in Gingival Crevicular Fluid and Plasma in Healthy and Diseased Periodontal Tissue in Presence or Absence of Obesity: A Clinico-biochemical Study

Guruprasad

Pradeep

2018

Bull. Tokyo Dent. Coll.

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Interleukin (IL)-34 has recently been identified as an alternative ligand for colonystimulating factor-1 receptor and plays an important role in osteoclastogenesis. The aim of this study was to assess and compare IL-34 levels in gingival crevicular fluid (GCF) and plasma in obese individuals in the presence or absence of periodontal disease and to determine whether they showed a correlation with disease severity. Forty patients aged between 25 and 40 yr were enrolled and categorized into 4 groups: 10 non-obese patients with healthy periodontium (Group I); 10 obese patients with healthy periodontium (Group II); 10 non-obese patients with chronic periodontitis (Group III); and 10 obese patients with chronic periodontitis (Group IV). Demographic variables such as age and body mass index score were recorded and assessed, together with clinical periodontal parameters such as the gingival index, probing pocket depth, and clinical attachment level scores in all groups. The GCF and plasma levels of IL-34 were quantified using enzyme-linked immunosorbent assay. The results showed that the mean IL-34 concentrations in GCF or plasma were highest in Group IV, followed by Group III, Group II, and Group I, with the difference among them being statistically significant (p<0.05). These results suggest that obese individuals with periodontitis have higher GCF and plasma IL-34 levels than non-obese individuals with healthy periodontium. This suggests IL-34 as a potential inflammatory marker of periodontal disease and obesity.

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“…The pro-inflammatory cytokines TNF-α and IL-1β regulate IL-34 expression in synovial and gingival fibroblasts by a mechanism involving NF-κB and MAPK 5,8) . Martinez 21) .…”

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Interleukin-34 Levels in Gingival Crevicular Fluid and Plasma in Healthy and Diseased Periodontal Tissue in Presence or Absence of Obesity: A Clinico-biochemical Study

Guruprasad

Pradeep

2018

Bull. Tokyo Dent. Coll.

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“…Since pro-inflammatory cytokines such as IL-1β and TNF-α play a crucial role in RA and since we previously demonstrated that TNF-α induces IL-34 expression, 5 we studied the effect of TGF-β1 and BMP-2 in inflammatory conditions. To this end, cells were treated with TNF-α.…”

Section: Tgf-β1 Inhibits Il-34 Expression In Inflammatory Conditionsmentioning

confidence: 99%

“…Its expression, correlated with inflammation, the number of leucocytes and the severity of the synovitis, is upregulated by TNFα and IL-1β. 5 TGF-βs and BMPs, are proteins involved in control of many biological processes such as cell proliferation and differentiation. The importance of TGF-β for the pathogenesis of arthritis is emphasized by several observations made in patients and in animal models.…”

Section: Introductionmentioning

confidence: 99%

Bone Morphogenetic Protein 2 and Transforming Growth Factor β1 Inhibit the Expression of the Proinflammatory Cytokine IL-34 in Rheumatoid Arthritis Synovial Fibroblasts

Chemel

Brion

Segaliny

et al. 2017

The American Journal of Pathology

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Bone‐ and Cartilage‐Protective Effects of a Monoclonal Antibody Against Colony‐Stimulating Factor 1 Receptor in Experimental Arthritis

Toh

Bonnefoy

Accart

et al. 2014

Arthritis & Rheumatology

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Objective. Colony-stimulating factor 1 receptor (CSF-1R) essentially modulates monocyte proliferation, migration, and activation, which are considered important for the pathogenesis of rheumatoid arthritis (RA). We undertook this study to determine CSF-1R expression in human RA as well as the efficacy of a specific anti-CSF-1R monoclonal antibody (AFS98) in 2 different animal models of RA.Methods. CSF-1R expression was examined in blood, synovium, and bone samples from RA patients, osteoarthritis (OA) patients, and healthy subjects. The efficacy of AFS98 was examined by clinical assessment, histology, and bone histomorphometry in collageninduced arthritis (CIA) and serum-transfer arthritis.Results. CSF-1R expression was increased in the synovium of RA patients compared to OA patients and healthy controls in fibroblast-like synoviocytes, follicular dendritic cells, macrophages, and osteoclasts. Circulating RA monocytes and neutrophils but not lymphocytes were CSF-1R؉. In mice, blockade of CSF-1R abrogated cartilage damage, bone erosion, and systemic bone loss, and this was associated with the depletion of osteoclasts in both models. While blockade of CSF-1R did not affect inflammation in passive serum-transfer arthritis, it significantly reduced inflammation in CIA, and this was associated with the absence of synovial macrophages and reduced splenic CD11b؉Gr-1؊ monocytes.Conclusion. CSF-1R was broadly expressed in human RA. Blockade of CSF-1R protected against bone and cartilage destruction in both mouse models and also showed significant antiinflammatory effects in the CIA model. These data provide evidence for CSF-1R as a therapeutic target in RA.Joint destruction in rheumatoid arthritis (RA) is mediated by inflammatory synovial tissue and subsequent osteoclastic bone resorption (1). This process is guided by inflammatory cytokines, which induce the expression of key factors involved in osteoclast differentiation. While numerous studies have shown the importance of RANKL in osteoclast-mediated bone resorption in both experimental inflammatory arthritis and human RA, data have been very limited to date concerning the role of the second essential factor for osteoclast differentiation, colony-stimulating factor 1 (CSF-1).The human CSF-1 receptor (CSF-1R; c-Fms) is a Drs. Toh, Bonnefoy, Haegel, Preville, Guillen, and Ancian and Ms Cochin, Mr. De Meyer, and Ms Thioudellet own stock or stock options in Transgene SA. Dr. Haegel and Ms Thioudellet are inventors of the anti-colony-stimulating factor 1 receptor monoclonal antibody CXIIG6 and its derivative, patents for which are assigned to Transgene SA.

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Interleukin 34 expression is associated with synovitis severity in rheumatoid arthritis patients

Abstract: This work for the first time identifies IL-34 expression in the synovial tissue of patients with arthritis. This cytokine, as a downstream effector of TNFα and IL-1β, may contribute to inflammation and bone erosions in RA.

Cited by 136 publications

References 17 publications

Interleukin-34 Levels in Gingival Crevicular Fluid and Plasma in Healthy and Diseased Periodontal Tissue in Presence or Absence of Obesity: A Clinico-biochemical Study

Interleukin-34 Levels in Gingival Crevicular Fluid and Plasma in Healthy and Diseased Periodontal Tissue in Presence or Absence of Obesity: A Clinico-biochemical Study

Bone Morphogenetic Protein 2 and Transforming Growth Factor β1 Inhibit the Expression of the Proinflammatory Cytokine IL-34 in Rheumatoid Arthritis Synovial Fibroblasts

Bone‐ and Cartilage‐Protective Effects of a Monoclonal Antibody Against Colony‐Stimulating Factor 1 Receptor in Experimental Arthritis

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