Assistant Professor, Department of Pediatric Disciplines
North Eastern Indira Gandhi Regional Institute of Health & Medical Sciences
Mawdiangdiang, Shillong *
Juvenile Idiopathic Arthritis (JIA) is a chronic inflammatory arthritis of childhood characterized by synovitis and systemic manifestations. Researches over the last decade have brought to light some of the important factors responsible for the
pathogenesis of the disease though knowledge about the etiology is still vague. T-cells, macrophages and B cells all have varying degrees of influence on the pathogenetic mechanisms. Cellular communication during inflammation occurs via direct cell to cell interaction or via soluble mediators. Many of these soluble mediators are glycoproteins designated as cytokines. A number of cytokines have been detected over the years such as Interleukins (IL), Interferons (IF), Tumor necrosis factor (TNF), Growth factors (GF), Colony stimulating factors (CSF) and chemokines. These cytokines are of two kinds - pro-inflammatory and anti-inflammatory and are responsible for regulating the magnitude, nature and duration of the inflammatory response. Unlike in adult onset rheumatoid arthritis, the cytokines involved in the pathogenesis of JIA and its subsets are still under evaluation.
Majority of the studies have demonstrated an increase in proinflammatory cytokines such as IL6, TNFa and IL1 in systemic onset JIA. Other studies have demonstrated that IL8 and IL18 are also raised in systemic onset JIA and IL8 in polyarticular JIA. On the other hand, anti-inflammatory cytokines such as IL10 have been demonstrated to be lower in patients with JIA indicating an enhanced pro-inflammatory response. The pattern of rise of these cytokines may form an important indicator of disease activity and have future implications for monitoring of patients with JIA. Characterization of these cytokines also have an implication for therapy as newer anti-cytokine molecules have become available for
treatment of these patients.
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