TNF-αPolymorphisms in Juvenile Idiopathic Arthritis: Which Potential Clinical Implications?

Sereno, Alessandra; Breda, Luciana; Laganà, Marta; Chiarelli, Francesco

doi:10.1155/2012/756291

Cited by 25 publications

(18 citation statements)

References 126 publications

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“…As mentioned in the Introduction, some of the JIA patients are known to be non‐responsive to Etanercept (Scardapane et al, ). Exercise or physical therapy of the jaw can act as a sophisticated, non‐invasive therapy to inhibit IL‐1/TNF‐α‐induced catabolic enzymes like MMP‐13.…”

Section: Discussionmentioning

confidence: 99%

Cyclic Tensile Strain Reduces TNF‐α Induced Expression of MMP‐13 by Condylar Temporomandibular Joint Cells

Tabeian

Bakker

Betti

et al. 2017

Journal Cellular Physiology

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To investigate whether the disproportionate degradation of mandibular condyle cartilage in arthritic juvenile temporomandibular joint (TMJ) is related to distinctive responses of TMJ-derived cells to tumor necrosis factor-α (TNF-α), and whether mechanical loading affects this response. The effect of TNF-α (0.1-10 ng/ml) was tested on juvenile porcine TMJ cells isolated from the condyle, fossa, and disc, grown in 3D agarose gels. Expression of anabolic and catabolic factors was quantified by RT-qPCR and/or immunohistochemistry. Condylar cells were stimulated for 12 h with TNF-α (10 ng/ml), followed by 8 h of 6% cyclic tensile strain, and gene expression of MMPs was quantified. TNF-α (10 ng/ml) reduced the expression of the matrix proteins collagen types I and II after 6 h of incubation. Aggrecan gene expression was increased in the presence of 0.1 ng/ml TNF-α. The fossa and disc cells responded to TNF-α with an increased expression of the aggrecanase ADAMTS4. TNF-α enhanced MMP-13 gene and protein expression only by condylar cells. Mechanical loading reduced this effect. Cells isolated from the different cartilaginous structures reacted differently to TNF-α. Since the disc and fossa contain a very low level of proteoglycans in comparison to the condyle, the role played by ADAMTS4 in degradation of the fossa and disc might be limited. TNF-α induced MMP-13 expression by condylar cells might be involved in the degradation of the juvenile condyle. Since this expression was reduced by mechanical loading, functional loading with oral physiotherapy or orthodontic activators may help to reduce the catabolic effect of TNF-α. J. Cell. Physiol. 232: 1287-1294, 2017. © 2016 Wiley Periodicals, Inc.

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Section: Discussionmentioning

confidence: 99%

Cyclic Tensile Strain Reduces TNF‐α Induced Expression of MMP‐13 by Condylar Temporomandibular Joint Cells

Tabeian

Bakker

Betti

et al. 2017

Journal Cellular Physiology

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“…Several studies have measured high amounts of TNF- α in the serum and synovial fluid of patients with rheumatoid arthritis and psoriatic arthritis and children with juvenile idiopathic arthritis [60–62]. Rheumatoid arthritis is an inflammatory disease caused by autoimmune responses, and it is aggravated by excessive bone resorption in the peripheral joints [63].…”

Section: Role Of Tnf-α In Joint Inflammation and Bone Destruction mentioning

confidence: 99%

Immunological Reaction in TNF-α-Mediated Osteoclast Formation and Bone ResorptionIn VitroandIn Vivo

Kitaura

Kimura

Ishida

et al. 2013

Clinical and Developmental Immunology

151

115

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Tumor necrosis factor-α (TNF-α) is a cytokine produced by monocytes, macrophages, and T cells and is induced by pathogens, endotoxins, or related substances. TNF-α may play a key role in bone metabolism and is important in inflammatory bone diseases such as rheumatoid arthritis. Cells directly involved in osteoclastogenesis include macrophages, which are osteoclast precursor cells, osteoblasts, or stromal cells. These cells express receptor activator of NF-κB ligand (RANKL) to induce osteoclastogenesis, and T cells, which secrete RANKL, promote osteoclastogenesis during inflammation. Elucidating the detailed effects of TNF-α on bone metabolism may enable the identification of therapeutic targets that can efficiently suppress bone destruction in inflammatory bone diseases. TNF-α is considered to act by directly increasing RANK expression in macrophages and by increasing RANKL in stromal cells. Inflammatory cytokines such as interleukin- (IL-) 12, IL-18, and interferon-γ (IFN-γ) strongly inhibit osteoclast formation. IL-12, IL-18, and IFN-γ induce apoptosis in bone marrow cells treated with TNF-α in vitro, and osteoclastogenesis is inhibited by the interactions of TNF-α-induced Fas and Fas ligand induced by IL-12, IL-18, and IFN-γ. This review describes and discusses the role of cells concerned with osteoclast formation and immunological reactions in TNF-α-mediated osteoclastogenesis in vitro and in vivo.

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“…In addition, the −308G genotype has been associated with better response to anti-TNF-α treatment in JIA patients, confirming adult data [17]. In some studies oligoarticular arthritis is significantly associated to the −238 SNP [10] [16] [18] [19].…”

Section: Introductionmentioning

confidence: 56%

“…An association between some TNF-α SNPs and adult rheumatoid arthritis susceptibility, severity and clinical response to anti-TNF-α treatment has been reported [10]- [13]. Furthermore, associations between TNF-α SNPs and subtypes of JIA have been found [12] [13].…”

Section: Introductionmentioning

confidence: 99%

Distinct Cytokine Profiles in Patients with Oligoarticular Juvenile Idiopathic Arthritis after in Vitro Blockade of Interleukin (IL)-1 and Tumor Necrosis Factor (TNF)-α

Kirchner¹,

Strothmann²,

Sonnenschein³

et al. 2014

WJV

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Oligoarticular juvenile idiopathic arthritis (oJIA) is an antigen-driven and lymphocyte-mediated autoimmune disorder with irregularity in the adaptive immune system. Auto reactive T cells, activated by cartilage-derived auto antigens, produce pro-inflammatory cytokines as IFN-γ and IL-17. Failure of regulatory T cells leads to decreased anti-inflammatory cytokine IL-10 production and results in the loss of immune tolerance. This activation of innate and adaptive immunity stimulates the release of pro-inflammatory cytokines IL-1, IL-6 and TNF-α. Thus, inhibition of these cytokines is considered as an appropriate therapeutic strategy for oJIA. The aim of this study was to investigate whether the blockade of a single cytokine pathway in the present cytokine setting causes an unfavourable imbalance in the cytokine system or whether the blockade is sufficient to suppress the inflammatory condition. We examined the cytokine secretion after in vitro inhibition of IL-1 and TNF-α of patients with oJIA and healthy subjects. This single center cohort study consisted of oJIA affected children and control subjects. Cytokine profiles from cell culture supernatants were examined with multiplex fluorescent bead immunoassay by flow cytometry. Adalimumab prevents highly effective and very selective effect of the cytokine TNF-α. Due to its structure, the mode of action of etanercept is difficult to display. In addition, adalimumab and etanercept appear in vitro suppressive to IFN-γ. The efficiency of both substances is particularly supported by the increased secretion of anti-inflammatory cytokine IL-4. In contrast, anakinra unselectively inhibits the pro-inflammatory macrophage cytokines. To conclude, our observations suggest that inhibition of IL-1 or TNF-α may contribute to the unselective decline of other pro-inflammatory cytokines in oJIA patients. The selective anti-inflammatory effect of cytokine inhibitors is most * Corresponding author. M. Kirchner et al. 111likely supported by an increase of IL-4 or IL-10. It still remains to be elucidated whether the reduced IFN-γ secretion is maybe causative for the increased susceptibility to infections with opportunistic pathogens.

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TNF-αPolymorphisms in Juvenile Idiopathic Arthritis: Which Potential Clinical Implications?

Cited by 25 publications

References 126 publications

Cyclic Tensile Strain Reduces TNF‐α Induced Expression of MMP‐13 by Condylar Temporomandibular Joint Cells

Cyclic Tensile Strain Reduces TNF‐α Induced Expression of MMP‐13 by Condylar Temporomandibular Joint Cells

Immunological Reaction in TNF-α-Mediated Osteoclast Formation and Bone ResorptionIn VitroandIn Vivo

Distinct Cytokine Profiles in Patients with Oligoarticular Juvenile Idiopathic Arthritis after <i>in</i> <i>Vitro</i> Blockade of Interleukin (IL)-1 and Tumor Necrosis Factor (TNF)-α

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TNF-αPolymorphisms in Juvenile Idiopathic Arthritis: Which Potential Clinical Implications?

Cited by 25 publications

References 126 publications

Cyclic Tensile Strain Reduces TNF‐α Induced Expression of MMP‐13 by Condylar Temporomandibular Joint Cells

Cyclic Tensile Strain Reduces TNF‐α Induced Expression of MMP‐13 by Condylar Temporomandibular Joint Cells

Immunological Reaction in TNF-α-Mediated Osteoclast Formation and Bone ResorptionIn VitroandIn Vivo

Distinct Cytokine Profiles in Patients with Oligoarticular Juvenile Idiopathic Arthritis after &lt;i&gt;in&lt;/i&gt; &lt;i&gt;Vitro&lt;/i&gt; Blockade of Interleukin (IL)-1 and Tumor Necrosis Factor (TNF)-α

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Distinct Cytokine Profiles in Patients with Oligoarticular Juvenile Idiopathic Arthritis after <i>in</i> <i>Vitro</i> Blockade of Interleukin (IL)-1 and Tumor Necrosis Factor (TNF)-α