In principle, inflammations are good for us – they indicate that our immune system is hard at work. Inflammations mount a defence against pathogens and then lead to the repair of destroyed tissue. However, if inflammations get out of control they may develop into a chronic form. Other immune and inflammatory cell types are then recruited to the inflammatory process, will severely harm healthy tissues and eventually destroy what they actually were supposed to protect.

A chronic inflammatory disease such as rheumatoid arthritis is a systemic autoimmune disorder, a disease that results when the immune system mistakenly attacks the body's own tissues. About 1% of the world's population is afflicted by rheumatoid arthritis that leads to both painful and long-term inflammations and to the destruction of the joints as well. In novel therapeutic approaches, scientists of this project were able to ameliorate substantially the symptoms of rheumatoid arthritis by interfering with the function of central inflammatory signalling mediators, e.g. the toll-like receptors or the MAP-kinase-kinase-kinase TAK1 (TGF beta-activated Kinase-1). Furthermore, they investigate calveolin-1 as a potential new target protein to intervene in inflammation in general and in infections with influenza viruses in particular.

Moreover, the scientists of this group were successful in isolating endothelial precursors from the pulmonary tissue of mice. These progenitor cells are capable to develop in vitro and in vivo into both blood- and lymphendothelial cells. The question here is which genes can be characterized as possible new candidates for therapeutic development.

The researchers of this group are concentrating on the issues mentioned before in four separate projects:

Priv.-Doz. Dr. Gerhard Gross

A novel gene therapeutic approach for rheumatoid arthritis by the systemic inhibition of a central inflammatory signaling mediator in the organism.

Dr. Manfred Wirth

The role of caveolin-1 in virus-cell interactions

Dr. Herbert A. Weich

Lymph and blood vessel formation during inflammation

Dr. Thomas Böldicke

Funktionelle Inhibierung von Zelloberflächen-und intrazellulären Rezeptoren mittels ER intrabodies

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