Interleukin‐1β and interleukin‐1 receptor antagonist gene polymorphisms in Korean patients with adult‐onset Still's disease

Jy, Youm; Jh, Woo; Kim, Tae Hee; Bae, Sang Cheol; Dh, Yoo

doi:10.1080/03009740701340081

Cited by 18 publications

(7 citation statements)

References 8 publications

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“…Further evidence for the contribution of IL-1 in AOSD pathophysiology came from the pioneering work by Pascual et al reporting that incubated peripheral blood mononuclear cells (PBMCs) with serum from patients with systemic form of juvenile idiopathic arthritis (SJIA), led to increased expression of innate immunity genes and release of large amounts of IL-1 β [27]. However, p ο lymorphisms in the IL-1 β and IL-1 receptor (IL-1R) genes have not been associated with AOSD susceptibility, at least in a Korean population [37]. Recent findings suggest activation of the protein complex nucleotide-binding oligomerization-domain-(NOD-) like receptor family, pyrin domain containing 3 (NLRP3) inflammasome, as an important source of IL-1 β ; this activation can occur by recognition of pathogen-associated molecular patterns (PAMPs) and danger-associated molecular patterns (DAMPs).…”

Section: Pathophysiologymentioning

confidence: 99%

Adult-Onset Still’s Disease: From Pathophysiology to Targeted Therapies

Mavragani

Spyridakis

Koutsilieris

2012

International Journal of Inflammation

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Adult-onset Still's disease (AOSD) is a systemic inflammatory disorder affecting primarily young individuals. The diagnosis is primarily clinical and necessitates the exclusion of a wide range of mimicking disorders. Given the lack of solid data in regard to the underlying pathogenetic mechanisms, treatment of AOSD has been for years largely empirical. Recent advances have revealed a pivotal role of several proinflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin-1 (IL-1), interleukin-6 (IL-6), interleukin-8 (IL-8), and interleukin-18 (IL-18) in disease pathogenesis, giving rise to the development of new targeted therapies aiming at optimal disease control.

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Section: Pathophysiologymentioning

confidence: 99%

Adult-Onset Still’s Disease: From Pathophysiology to Targeted Therapies

Mavragani

Spyridakis

Koutsilieris

2012

International Journal of Inflammation

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“…Anyway, infection alone is unlike to be sufficient to trigger AOSD, and a predisposing genetic background is probably required even if no consistent associations with HLA aplotypes have been individuated [23]. Youm et al have studied 83 AOSD patients to investigate whether IL-1 β and IL-1Ra gene polymorphisms are associated with the development and clinical features of AOSD, but no differences were observed between patients and healthy controls [24]. A potent IL-1 β production-inducer is IL-18, a member of the IL-1 family that growing evidences are demonstrating to be pivotal in promoting the systemic inflammatory process of AOSD.…”

Section: Il-1β In Aosd Pathogenesismentioning

confidence: 99%

Anti-Interleukin-1 Agents in Adult Onset Still's Disease

Giampietro

Fautrel

2012

International Journal of Inflammation

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Interleukin 1β(IL-1β) is emerging as a master mediator of adult onset Still’s disease (AOSD) pathogenesis. This pleiotropic cytokine, whose expression is under the control of the inflammasome pathway, has a wide type of effects. As a key mediator of innate immunity is a potent pyrogen and facilitates neutrophilic proliferation and diapedesis into the inflamed tissues, which are key AOSD manifestations. The study of proinflammatory cytokines profiles in sera and pathological tissues of AOSD patients has shown elevated levels of IL-1β, these levels being highly correlated with disease activity and severity. These experimental evidences and the analogy with other autoinflammatory diseases that share with AOSD clinical and biological characteristics have suggested the blockade of IL-1βas a possible new therapeutic option for the AOSD, especially in conventional therapy resistant cases. Anakinra, the first anti-IL-1 agent put on the market, has demonstrated capable to induce a rapid response sustained over time, especially in systemic forms, where anti-TNFαfailed to control symptoms. While a growing number of evidences supports the utilisation of anakinra in AOSD, a new generation of anti-IL1βantagonists is developing. Canakinumab and rilonacept, thanks to their higher affinity and longer half-life, could improve the management of this invalidating disease.

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“…SoJIA is not associated with HLA variants, but sequence polymorphisms in several pro-and anti-inflammatory cytokines, such as IL-6, TNF-α, IL-1β, IL-1RA, and IL-10, have been reported. This suggests dysregulation of the balance between pro-and anti-inflammatory signals, resulting in systemic inflammation [14][15][16][17][18][19].…”

Section: Genetic Associations In Aidmentioning

confidence: 99%