Spondyloarthritis (SpA) is a chronic inflammatory rheumatic disorder, with few effective treatments such as TNF blockers which can temporarily suppress inflammation, but none has yet proven to affect long-term disease outcome. There is a deep need to better understand pathological mechanisms controlling both initiation and progression of SpA.
During the last 10 years multiple large scale studies including genome-wide genetic and gene expression analysis. These approaches are highly powerful to identify new genetic determinants and molecular mechanisms potentially involved in the disease but they also demonstrated some limits showing that there is a need to rethink these approaches in a more integrated view.
In this presentation we will discuss the potential utility of such approach, and present data illustrating the comparison between molecular signatures obtained in human cells as well as in animal model of SpA and how to link genetic studies to gene expression studies.
Disclosure of Interest None declared