Fc gamma receptor mediated modulation of dendritic cells as a potential strategy in the battle against rheumatoid arthritis.
SourceNetherlands Journal of Medicine, 64, 4, (2006), pp. 103-108
Article / Letter to editor
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Netherlands Journal of Medicine
SubjectN4i 1: Pathogenesis and modulation of inflammation; N4i 4: Auto-immunity, transplantation and immunotherapy; NCEBP 2: Evaluation of complex medical interventions; NCMLS 1: Infection and autoimmunity; UMCN 4.2: Chronic inflammation and autoimmunity
Autoimmune diseases such as rheumatoid arthritis (RA) result from a deregulation of immune responses culminating in immune-mediated tissue injury. In RA, this tissue injury is mainly reflected by synovitis and subsequent joint damage, although involvement of visceral organs (heart, lungs and kidneys) often leads to severe comorbidity. Accumulating evidence points towards dendritic cells (DC) as the principal regulators of the balance between immunity and tolerance. Recently, a large body of evidence has demonstrated that the balance between activating and inhibitory Fc gamma receptor (Fc gammaR) subtypes is intricately involved in the regulation of DC behaviour. In this overview we summarise recent findings from our group and others that suggest an important role for Fc gammaR in arthritis. Furthermore, we postulate novel mechanisms of how triggering of Fc gammaR might be used to manipulate DC function and combat autoimmunity. When DC are envisaged as useful targets in the light of DC immunotherapy in RA, detailed knowledge on the regulatory pathways of Fc gammaR in RA is of paramount importance.
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