Regular articleA POSSIBLE ROLE FOR SOLUBLE IL-6 RECEPTOR IN THE PATHOGENESIS OF SYSTEMIC ONSET JUVENILE CHRONIC ARTHRITIS
References (0)
Cited by (73)
Role of interleukin-6 and pentraxin 3 as an early marker in Peyronie's disease
2017, Kaohsiung Journal of Medical SciencesCitation Excerpt :For example, IL-6 has been demonstrated to play a critical role in the pathogenesis of systemic sclerosis, an autoimmune connective tissue disorder characterized by fibrosis of the skin and internal organs [23]. Elevated IL-6 levels were detected in serum and synovial tissues of patients with rheumatoid arthritis and also in the serum of patients with inflammatory disorders including asthma, psoriasis, inflammatory bowel disease, and Crohn's disease [24–28]. PTX3 is a multifunctional fluid-phase pattern recognition receptor that links innate immunity, inflammation, and matrix deposition, and shows a unique pattern of regulation [29].
Alternative intronic polyadenylation generates the interleukin-6 trans-signaling inhibitor sgp130-E10
2014, Journal of Biological ChemistryCitation Excerpt :Although sgp130Fc inhibited STAT3 phosphorylation at concentrations of ∼1 nm, even 100 times more sgp130-E10Fc only reduced, but did not completely inhibit, STAT3 phosphorylation (Fig. 6D). Hyper-activation of gp130 by IL-6 trans-signaling is due to elevated levels of IL-6 and sIL-6R and was observed in many inflammatory disorders, e.g. in rheumatoid arthritis (20–22). IL-6 trans-signaling is crucial for the development and maintenance of rheumatoid arthritis (23, 24).
Targeting interleukin-6 in inflammatory autoimmune diseases and cancers
2014, Pharmacology and TherapeuticsCitation Excerpt :RA is an autoimmune disease that results in chronic, progressive inflammatory disorders of the joints and surrounding tissues, often leading to irreversible joint damage and systemic complications (Smolen et al., 2007). High levels of IL-6/sIL-6R complex in synovial fluids in patients with RA and juvenile RA are associated with joint destruction and disease progression (Keul et al., 1998). IL-6 produced by bone marrow stromal cells can induce the receptor activator of NF-κB ligand (RANKL), which is critical for the differentiation and activation of osteoclasts and bone resorption (Palmqvist et al., 2002).
Rational development and utilization of antibody-based therapeutic proteins in pediatrics
2013, Pharmacology and TherapeuticsCitation Excerpt :Since JIA encompasses a group of clinically heterogeneous arthritides, the contribution of proinflammatory cytokines to disease formation is likely different among different subsets of patients (Ravelli & Martini, 2007). For example, studies have shown that IL-6 and IL-1 play a much larger role in the disease manifestations of systemic JIA than they do for polyarticular JRA (Keul et al., 1998; Pascual et al., 2005; Ruperto et al., 2012). This knowledge provides a biologic explanation as to why anti-TNFα therapies have been less effective in patients with systemic JIA (Kimura et al., 2005).
Interleukin-6: From an inflammatory marker to a target for inflammatory diseases
2012, Trends in ImmunologyCitation Excerpt :Furthermore, blocking the IL-6R in wild-type mice reduces the development of arthritis in the CIA model [29], suggesting that this treatment could be used for clinical therapy. In addition to IL-6, the levels of sIL-6R are also elevated in RA and juvenile RA, and these levels are associated with joint destruction and disease progression [26,30], providing more evidence that IL-6 contributes to the disease. sIL-6R at sites of inflammation could confer IL-6 responsiveness to cells that do not express an IL-6R (e.g., osteoclasts and fibroblasts).
- f1
Correspondence to: P. Woo, Department of Molecular Pathology, University College London Medical School, The Windeyer Institute of Medical Sciences, 46 Cleveland Street, London W1P 6DB, UK; E-mail: [email protected]