Juvenile idiopathic arthritis (JIA), joint inflammation with unknown cause in children, affects an estimated 250,000 children in the US alone. About 10% of these cases begin with fevers and/or rash that precede joint symptoms by months or years, a subset called systemic onset JIA (SoJIA). These are hard to diagnose and most do not respond to TNF blockade, a therapy that helps many adult rheumatoid arthritis patients. Here, Pascual and colleagues show that the disease is instead driven by the other major proinflammatory cytokine, interleukin 1 (IL-1). They found that activate peripheral blood leukocytes from SoJIA patients make more IL-1 than do those from healthy people. Sera from SoJIA patients increased the expression of immune-related genes by leukocytes from healthy people. Most strikingly, an IL-1 receptor antagonist (IL-1Ra, Anakinra) reduced fever, arthritis, and other symptoms or markers of disease in all 9 SoJIA patients treated.
Pascual et al., J Exp. Med. 201(9) 1479-1486.
Sunday, January 21, 2007
Interleukin-1 in Systemic Juvenile arthritis
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IL-6 implicated in SoJIA
This paper [nih.gov] by Miyamae et al. reports examining the sera of 8 SoJIA patients who responded to "conventional therapy" (steroids and NSAIDs (non-steroidal anti-inflammatory drugs)) and 15 who did not respond. The non-responders did respond to an experimental therapy with an antibody the the IL-6 receptor (MRA). They found reproducible differences in the sera of patients before vs. after treatment. Most of the differences were observed with both treatments, suggesting they may be good markers of the disease process (instead of a treatment effect). One of these markers was serum amyloid A, which was already known to be associated with SoJIA.
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