Identification of therapeutic targets and antisense oligonucleotide mediated exon skipping based therapies in arthritis

Abstract

Rheumatoid arthritis (RA) is a chronic inflammatory joint disease leading to

destruction of cartilage and bone. The inflammation in the joints is mainly caused by

inflammatory cytokines that are over-produced by various types of immune cells. Artritis is an autoimmune disease that is characterized by the presence of autoantibodies. These autoantibodies form immune complexes (IC) which are other important players in joint inflammation because they activate various immune cells by binding to Fc receptors (FcR). Binding and activation of FcRs initiates intracellular signaling that triggers activation and release of various inflammatory mediators. In this thesis we describe a variety of aspects of arthritis research that has been performed to get a better understanding of the underlying molecular and cellular disease mechanisms and to develop novel therapeutic strategies.