Abstract
Monocytes (Mos) and macrophages (Mφs) are key players in the innate immune system and are critical in coordinating the initiation, expansion, and regression of many autoimmune diseases. In addition, they display immunoregulatory effects that impact inflammation and are essential in tissue repair and regeneration. Juvenile idiopathic arthritis (JIA) is an umbrella term describing inflammatory joint diseases in children. Accumulated evidence suggests a link between Mo and Mφ activation and JIA pathogenesis. Accordingly, topics regarding the signals and mechanisms regulating Mo and Mφ activation leading to pathologies in patients with JIA are of great interest. In this review, we critically summarize recent advances in the understanding of how Mo and Mφ activation is involved in JIA pathogenesis and focus on the signaling pathways and mechanisms participating in the related cell activation processes.
Highlights
Overview of the Pathogenesis of Juvenile Idiopathic ArthritisJuvenile idiopathic arthritis (JIA) is the leading chronic rheumatic disease of childhood and occurs in children before their sixteenth birthday with symptoms of articular inflammation for at least 6 weeks [1]
Evidence suggests a distinct pathogenesis of systemic onset juvenile idiopathic arthritis compared to that of the oligoarticular and polyarticular forms of JIA [4]. sJIA is an autoinflammatory disease marked by universal inflammation due to a dysregulated innate immune system [2,7,8]
We critically summarize recent advances in the understanding of how Mo and Mφ activation is involved in JIA pathogenesis and focus on the signaling pathways and mechanisms participating in the related cell activation processes
Summary
Juvenile idiopathic arthritis (JIA) is the leading chronic rheumatic disease of childhood and occurs in children before their sixteenth birthday with symptoms of articular inflammation for at least 6 weeks [1]. Evidence suggests a distinct pathogenesis of systemic onset juvenile idiopathic arthritis (sJIA) compared to that of the oligoarticular and polyarticular forms of JIA [4]. Mos/Mφs are important players in the innate immune system and are critical in coordinating the initiation, expansion, and resolution of many autoimmune diseases [8]. They possess a wide range of inflammatory, immunomodulatory, and tissue-repairing capacities via their secretion of numerous proinflammatory cytokines, growth factors, and proteolytic enzymes to stimulate and recruit effector cells to inflamed tissues [7,8,9]. We critically summarize recent advances in the understanding of how Mo and Mφ activation is involved in JIA pathogenesis and focus on the signaling pathways and mechanisms participating in the related cell activation processes
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