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RA IV Zelluläre Immunregulation


In the 1st FP, major progress has been made in the understanding of inflammatory bowel disease, vasculitis, atopic eczema, asthma and cutaneous inflammation mediated by autoimmunity to type VII collagen. IL-6 trans-signaling was recognized as the mechanism of chronicity in pro-inflammatory IL-6 activation. Therefore, a specific IL-6 trans-signaling blocker was developed within the Cluster, which will reach clinical trials in 2012 and will lead to a new personalized concept for therapy. The RA described here defines cellular and molecular pathways controlled by the new disease risk alleles discovered in 1st FP. This RA will intensely collaborate with CL VII “Human Immunophenotyping” and CL XII “Mouse Model Systems of Inflammation”. Therefore, this RA will provide a mechanistic link between identified risk genes and the development of novel diagnostic and therapeutic strategies.

Contribution to the Scientific Discourse

The RA investigates complex interactions of immune and non-immune cells and cellular activation programs in physiological inflammatory responses and barrier diseases. The joined research projects in this broad field are focused on existing expertise areas (e.g. IL-6, autoreactive B cells) and comprise: (1) complex in vitro and in vivo models that study mechanisms of onset, perpetuation and termination in inflammation and barrier disruption, (2) studies on the link between molecular pathways originating from disease genes and general inflammation mechanisms and (3) approaches to understand and therapeutically modulate primary inflammation pathophysiology in proximity to etiologic causations.

Figure: Cellular and molecular mechanisms will be identified that regulate the pathogenesis of in-flammatory barriers diseases with a focus on the interaction between pro-and anti-inflammatory signals and barrier disruption

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