SFB-TRR43

The scientific basis of the supra-regional organised CRC between Berlin and G�ttingen, in which five different institutions participate, is the only recently accepted insight that immunological processes are not only involved in classical inflammatory disorders of the nervous system such as multiple sclerosis (MS), but also appear to play a major role in the pathogenesis of primarily non-inflammatory or rather �atypical� neuroimmunological pathologies, such as stroke � both ischemic and hemorrhagic �, brain tumors, and neurodegenerative disorders. In any of these conditions or disorders, immune cells interact with cells of the nervous system via complex signalling cascades. Besides a local crosstalk between cells of the nervous and the immune systems there is increasing evidence that CNS alterations in turn also impact systemic immune responses, which may facilitate either life-threatening (systemic) infections or protect CNS tissue by modulating local CNS actions. Although the initiating, pathogenetically relevant events may differ considerably between various CNS diseases, they seem to utilize common pathways in the (bidirectional) crosstalk between the immune and the nervous system. Deciphering these common pathways is an essential bond and common denominator of the CRC TRR 43 consortium in order to enable the design of regimens that modulate various CNS diseases irrespective of their specific pathogenesis or etiology.

The key questions we seek to answer are as follows:

When, why and how do immune cells enter the CNS and interact with, or even attack, neural cells?
Is there a common denominator of the immune response in various CNS pathologies, irrespective of the specific pathogenesis or origin, and does it rather sustain damage or � at least in specific situations � promote repair?

Spokesperson (Berlin) - Prof. Dr. Frank Heppner

Deputy Spokesperson (Göttingen) - Prof. Dr. Wolfgang Brück