Neuroimmunology Seminar Series
at the University of Virginia
Sponsored by
Michael K. Racke, M.D.
Professor and Chairman of Neurology
The Helen C. Kurtz Chair in Neurology
The Ohio State University Medical Center
Transcriptional Regulation of Encephalitogenic T Cells
Thursday, May 22nd, 2:00 p.m., Jordan 1-17
Zsuzsanna Fabry, Ph.D.
Chair, Cellular and Molecular Pathology Graduate Program,
Department of Pathology and Laboratory Medicine
University of Wisconsin-Madison School of Medicine and Public Health
Neuroinflammation in the Central Nervous System
Tuesday, April 22nd, 2008, 4:00, Jordan 1-5
Hosted by the Departments of Neuroscience and the Neuroscience Graduate Program
Richard Ransohoff, M.D.
Professor, Department of Molecular Medicine & Pathology
Director, Neuroinflammation Research Center, Department of Neuroscience
Chemokines in the CNS: Much More Than Leukocyte Trafficking
Thursday, March 27, 2008, 2:00 pm, Jordan 1-14
Hosted by Jonathan Kipnis, Department of Neuroscience
Uwe-Karsten Hanisch
Institute of Neuropathology, University of Goettingen, Germany
Microglial Activation by TLR Ligands: Usual and Unusual Suspects
Thursday, March 6, 2008, 12:30 pm, Jordan 1-14 CANCELLED
Hosted by Jonathan Kipnis, Department of Neuroscience
Institute of Neuropathology, University of Goettingen, Germany
Microglial Activation by TLR Ligands: Usual and Unusual Suspects
Thursday, March 6, 2008, 12:30 pm, Jordan 1-14 CANCELLED
Hosted by Jonathan Kipnis, Department of Neuroscience
To sense environmental signals, microglial cells are equipped with an array of receptors. They also express several Toll-like receptors (TLR) and mount diverse responses to their agonists. We focussed on a protein tyrosine kinase activity which is involved in the signalling of various TLR. The PTK assists the MyD88 route and controls the intracellular calcium, thereby affecting activation-associated functions. Moreover, TLR may serve the recognition of a broader variety of signals indicating homeostatic disturbance. We identified endogenous proteins which apparently activate microglia through a TLR4/MyD88-dependent mechanism. LPS, the prototypic microbial ligand of TLR4, can be ruled as a confounding factor. The ability of the ligands to trigger TLR4 signalling seems to depend on critical structural requirements. Interestingly, although the ligands use TLR4 for mandatory signalling, additional (receptor) components appear to fine- tune respective consequences. TLR4 may thus serve responses to different microglia-challenging stimuli but the induced responses distinguish between individual agonists.