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 (FcγR) 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 FcγR in arthritis. Furthermore, we postulate novel mechanisms of how triggering of FcγR 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 FcγR in RA is of paramount importance.