Neutrophils: the forgotten cell in JIA disease pathogenesis

Jarvis, James N.; Jiang, Kaiyu; Petty, Howard R.; Centola, Michael

doi:10.1186/1546-0096-5-13

Cited by 24 publications

(24 citation statements)

References 53 publications

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“…IL-1 and IL-6, which originate from activated monocytes, are triggered by TNFs. These cytokines have been shown to be up-regulated during ongoing periods of ERA disease and, moreover, are related to local inflammation [9,11,66]. Before beginning etanercept treatment, high expression of MCP-1/CCL2 and MIG chemokines, produced primarily by activated T cells, was noted in both ERA subjects.…”

Section: Discussionmentioning

confidence: 92%

Proteomic Analysis of Plasma to Reveal the Impact of Short-Term Etanercept Therapy in Pediatric Patients with Enthesitis-Related Arthritis: A Case Report

Chen

Wang²,

Pan³

et al. 2010

CCHTS

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In a variety of countries, juvenile idiopathic arthritis (JIA) is the most common cause of chronic arthritis in childhood, yet its etiology is still unknown. In recent years, etanercept, an effective inhibitor of tumor necrosis factor alpha (TNF-alpha), was used as an alternative in certain oligoarticular JIA patients resistant to conventional nonsteroidal anti-inflammatory drugs (NSAIDs), disease-modifying anti-rheumatic drugs (DMARDs), and corticosteroid therapies, and it resulted in sustained improvement in JIA symptoms. This pilot study explores the alterations of specific panels of cytokines and protein profiles in plasma for two Taiwanese pediatric cases with diagnosed enthesitis-related arthritis (ERA), a type of JIA. The patients were studied before and after taking etanercept alone, using a high-content screening approach employing membrane-based human cytokine antibody microarray and the conventional two-dimensional gel electrophoresis (2-DE) proteomic technique. Specifically, 2-DE in combination with mass spectrometry (MALDI-MS) revealed the functional roles of plasma proteins associated with the regulation of immune responses during short-term etanercept treatment of children with ERA. Our study shows that this biotherapy improved clinical ERA manifestations through the regulation of inflammatory mediators, including several cytotoxic cellular cytokines (IL-2/IFN-g), chemokines (MCP-1), and growth factors (GRO) that affect the expression of specific acute phase proteins such as haptoglobins, immunoglobulin A, and fibrinogen-gamma chain. Meanwhile, an up-regulation of antithrombin chain I, vitamin-D binding protein (VDBP), and the various apolipoproteins was also observed after the administration of etanercept in both studied children. These results may be interpreted as the relevant predictive biomarkers of therapeutic responses to etanercept. They suggest that etanercept, which is still rarely used in Taiwan, is a viable treatment for JIA patients, without adverse health effects and increased risk of secondary infections.

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Section: Discussionmentioning

confidence: 92%

Proteomic Analysis of Plasma to Reveal the Impact of Short-Term Etanercept Therapy in Pediatric Patients with Enthesitis-Related Arthritis: A Case Report

Chen

Wang²,

Pan³

et al. 2010

CCHTS

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“…Indeed, as knowledge of CD4 + T cell subsets has grown, models of their involvement in oligoarticular and polyarticular JIA have been refined and support the idea that mechanistic differences exist. Available evidence also argues that antigen-driven autoimmunity is insufficient to explain all the features of oligoarticular and polyarticular JIA,(31) and implicate the involvement of both innate and adaptive immune responses. These issues are the focus of the rest of this Review.…”

Section: Pathogenesismentioning

confidence: 99%

Oligoarticular and polyarticular JIA: epidemiology and pathogenesis

et al. 2009

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Summary Juvenile idiopathic arthritis (JIA) refers to a group of chronic childhood arthropathies, currently classified into subtypes primarily on the basis of clinical features. Research has focused on the hypothesis that these subtypes arise through distinct etiologic pathways. In this Review, we discuss four subtypes of JIA: persistent oligoarticular, extended oligoarticular, rheumatoid-factor positive polyarticular and rheumatoid-factor-negative polyarticular. These subtypes differ in prevalence between ethnic groups and are associated with different HLA alleles. Non-HLA genetic risk factors have also been identified, some of which reveal further molecular differences between these subtypes, while others suggest mechanistic overlap. Investigations of immunophenotypes also provide insights into subtype differences: adaptive immunity appears to have a prominent role in both polyarticular and oligoarticular JIA, and the more-limited arthritis observed in persistent oligoarticular JIA as compared with extended oligoarticular JIA may reflect more-potent immunoregulatory T-cell activity in the former. Tumor necrosis factor seems to be a key mediator of both polyarticular and oligoarticular JIA, especially in the extended oligoarticular subtype, although elevated levels of other cytokines also are observed. Limited data on monocytes, dendritic cells, B cells, natural killer T cells, and neutrophils suggest that the contributions of these cells differ across subtypes of JIA. Within each subtype, however, common pathways appear to drive joint damage.

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“…56 In recent years, neutrophils have received attention for their possible role in initiating the inflammation of JIA. Jarvis et al, 57 suggest that innate immunity, particularly neutrophils, may have been overlooked in JIA pathogenesis. Neutrophil-derived S100 proteins may serve as a useful marker for response to treatment.…”

Section: ' Pathogenesismentioning

confidence: 98%