Project Details
TRR 43: The Brain as a Target of Inflammatory Processes
Subject Area
Medicine
Term
from 2008 to 2016
Project identifier
Deutsche Forschungsgemeinschaft (DFG) - Project number 29837756
In the past 5 years, our understanding of the implications and the importance of immune processes contributing to CNS diseases has progressed at a remarkable pace. In order to better facilitate the translation of the findings to the human situation, the understanding of immune mechanisms by dissecting the molecular cues of neuroimmune signaling pathways is necessary. We know now that immune actions are not only involved in prototypical inflammatory brain diseases such as multiple sclerosis (MS) or encephalitides, but also play an important role in the pathogenesis and pathology of central nervous system (CNS) disorders that are generally considered to be primarily noninflammatory, such as stroke, brain tumors and neurodegenerative disorders, such as Alzheimer's disease.Although the initiating events may differ considerably between various CNS diseases, they seem, at least in some instances, to utilize common pathways for the cross talk between the immune and the nervous systems. Deciphering these common - or divergent - pathways is a common denominator for the research of the Collaborative Research Centre consortium. While insights into immune functions in certain CNS diseases have already opened up new avenues for preventing or treating these diseases, the Collaborative Research Centre envisages transferring knowledge of immune actions in a given CNS disease to CNS disorders with different origins but similar immune actions. Recent insights have led to a discrimination of CNS disorders as having either an innate-immune or an adaptive-immune component. The Collaborative Research Centre has been at the forefront of exciting discoveries as to the importance of immune processes in CNS diseases, and will thus continue its successful approach. Only recently it became clear how essential it is to engage researchers of a variety of educational backgrounds in the efforts to develop a coherent physiological and pathophysiological description of the innate and adaptive immune actions in CNS disorders, and to translate new insights into research and treatment strategies. The most difficult questions in the field can often be most effectively addressed when investigators with different educational background share a fundamental understanding of complex organ systems and - as shown in this Collaborative Research Centre - synergistically cooperate in the best possible way.
DFG Programme
CRC/Transregios
Completed projects
- A01 - The role of innate immune receptors in neurodegeneration (Project Head Lehnardt, Seija )
- A03 - Role of inflammation for long-term post-stroke outcome (Project Heads Dirnagl, Ulrich ; Endres, Matthias )
- A04 - Control of microglial function by activation of neurotransmitter/-hormone receptors (Project Heads Kettenmann, Helmut ; Wolf, Susanne A. )
- A05 - Phenotypic diversity of microglia (Project Heads Brück, Wolfgang ; Hanisch, Uwe-Karsten )
- A06 - Dissecting mechanisms of immune actions in Alzheimer's disease (Project Head Heppner, Frank )
- A07 - Differential roles of resident microglia and myeloid cells in neuroinflammatory conditions (Project Heads Priller, Josef ; Prinz, Marco )
- A08 - Analysis of immediate cellular response cascades upon defined CNS lesions by in vivo two-photon laser-scanning microscopy (Project Head Kirchhoff, Frank )
- A09 - Activation of the Inflammasome in Amyotrophic Lateral Sclerosis (Project Head Zychlinsky, Arturo )
- A10 - Connecting myelin membrane turnover with antigen presenting cells and autoimmunity (Project Head Simons, Mikael Jakob )
- B02 - Mechanisms and sites of neurodegeneration in chronic inflammation of the brain (Project Head Zipp, Frauke )
- B03 - Strategies of neuronal self-defence, role of neuronal MHC class I in determining susceptibility to CTL attack and neuroplasticity (Project Head Merkler, Doron )
- B04 - Mechanisms and functional role of immune response following axonal lesion (Project Heads Brandt, Christine ; Nitsch, Robert )
- B05 - Role of CNS antigen-specific T cell responses for regeneration and functional outcome after stroke and impact of post-stroke infections (Project Heads Meisel, Andreas ; Meisel, Christian Alexander )
- B06 - Secondary neuroinflammation in the CNS white matter and its modulation by erythropoietin (Project Heads Ehrenreich, Hannelore Maria ; Nave, Ph.D., Klaus-Armin )
- B07 - The role of immunoproteasomes and the ubiquitin system in inflammatory processes in mouse models of Alzheimer's and Parkinson's disease (Project Heads Aktas, Orhan ; Heppner, Frank ; Kloetzel, Peter Michael ; Krüger, Elke Beate )
- B09 - Axonal and neuronal damage as pathological substrates of disease progression in MS (Project Heads Brück, Wolfgang ; Stadelmann-Nessler, Christine )
- B10 - Encephalitogenic T cells during preclinical EAE: migratory behavior and functional analysis of fluorescent GFP-transduced T cells (Project Heads Flügel, Alexander ; Odoardi, Francesca )
- B11 - Intravital analyses of T cell priming and effector phases during active and spontaneous EAE (Project Heads Flügel, Alexander ; Lühder, Fred )
- B12 - Cerebral Spreading Inflammation (CSI) after Acute Subarachnoid Hemorrhage (aSAH) - An Intraparenchymal Reaction to an Extraparenchymal Disease (Project Head Vajkoczy, Peter )
- B13 - Role of CD8+ T cells in neuroinflammation and damage in a rat model of RRMS (Project Head Reichardt, Holger M. )
- C01 - Central tasks / Administrative office of the SFB TRR 43 (Project Heads Heppner, Frank ; Zipp, Frauke )
- MGK - Integrated Research Training Group (Project Heads Hanisch, Uwe-Karsten ; Kettenmann, Helmut )
Applicant Institution
shared FU Berlin and HU Berlin through:
Charité - Universitätsmedizin Berlin
Charité - Universitätsmedizin Berlin
Co-Applicant Institution
Freie Universität Berlin; Georg-August-Universität Göttingen; Humboldt-Universität zu Berlin
Participating Institution
Max-Delbrück-Centrum für Molekulare Medizin (MDC); Max-Planck-Institut für Infektionsbiologie; Max-Planck-Institut für experimentelle Medizin (aufgelöst)
Spokesperson
Professor Dr. Frank Heppner