Diego Kyburz has an international reputation as researcher on the pathogenesis of rheumatoid arthritis. His achievements include the demonstration of endogenous Toll-like receptor 3 ligands in the synovium of patients with rheumatoid arthritis and the first description of a dysregulation of microRNA expression in rheumatoid arthritis. He has been invited to give lectures at international meetings in the US and Europe. He was awarded a fellowship by the SSMBS and several project grants by the Swiss National Fund. DK’s publications have been cited 1’847 times; his h-index is 21 (Web of Science).

Prof. Kyburz has accepted a Professorship at the University of Basel and left the consortium in the course of 2014. 

In the framework of KFSP Small RNAs, Prof. Kyburz investigated questions related to chronic arthirits:   

Chronic joint inflammation in patients with rheumatoid arthritis (RA) results in progressive destruction of cartilage and bone, leading to severe pain and ultimately loss of function and disability. The synovial cells typically show an activated phenotype characterized by overexpression of proinflammatory cytokines, chemokines as well as matrix-degrading enzymes. The initial trigger of the disease is not known, however the formation of autoantibodies and the HLA-association suggest that RA is an autoimmune disease. Activation of the innate immune system seems to be an early event in the disease pathogenesis as increased expression of toll-like receptors (TLR) on synovial cells can be found already at very early stages of disease. As endogenous ligands of TLR are present in inflamed and damaged joints this may lead to sustained inflammation by activation of synovial cells in a vicious circle. No gene polymorphisms of innate immune receptors have so far been identified to be associated with RA.

However, evidence for a dysregulation of gene expression regulation at the posttranscriptional level has emerged. In a previous project funded by the Swiss National Fund we have analysed microRNA expression in synovial cells of patients with RA and have reported a dysregulation of selected microRNA in this disease. Although data on dysregulated expression of microRNA in various diseases are accumulating, the functional impact of these microRNA remain unclear in many instances.

Our group is interested to address the following scientific questions:

• How do microRNA control important pathways of inflammation in chronic arthritis?
• Identification of microRNA or combinations of microRNA within anti-inflammatory effects on synovial cells
• What is the functional role of microRNAs targeted by adipokines in synovial cells
• Do microRNA expressed in the peripheral blood cells or serum have potential as markers for rheumatoid arthritis and risk for cardiovascular complications