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Pathogenesis of juvenile idiopathic arthritis 

Pathogenesis of juvenile idiopathic arthritis
Chapter:
Pathogenesis of juvenile idiopathic arthritis
Source:
Oxford Textbook of Rheumatology (4 ed.)
Author(s):

David Bending

, Kiran Nistala

, Lucy R. Wedderburn

, and Elizabeth C. Rosser

DOI:
10.1093/med/9780199642489.003.0060_update_002
Previous versions of this chapter are available. To view earlier versions of this chapter view the full site here.

Although the term juvenile idiopathic arthritis (JIA) encompasses a heterogeneous group of diseases, they all share a common pathological hallmark: inflammation of the synovium. Highly activated T cells, monocytes, and neutrophils are attracted to the joint and secrete mediators that not only perpetuate inflammation, but also may attenuate immune regulation. In the oligoarticular and polyarticular forms of JIA, which are thought to be autoimmune conditions, dysregulated adaptive immunity is a likely factor in disease pathogenesis; the nature of the interactions between T-effector cells (Teffs) and T-regulatory cells (Tregs) is probably a key factor in controlling disease progression. Factors that affect the frequency and function of Tregs and/or the sensitivity of Teffs to mechanisms of immune suppression will therefore impact the disease course. In the systemic form of JIA, however, dysregulation of innate immune pathways appears more central to disease pathogenesis, resulting in augmented levels of interleukins IL-1β‎, IL-6, and IL-18. In the end, a final common pathological pathway in JIA is the activation of monocytes and neutrophils which are the principal mediators of joint inflammation and damage. This is supported by the fact that the therapies that have targeted innate cytokine pathways have shown greater success in the treatment of JIA.

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