Winter Semester 2017, NIC 2

Winter Semester 2017-NIC 2







January 23rd


Winter Semester 2017

Mondays at 14:00h

Charité Mitte Campus – Universitätsmedizin Berlin

Ferdinand Sauerbruch Hörsaal 4, Hufelandweg 6


 Volker Siffrin, MD

Max-Delbrück-Centrum for Molecular Medicine, Berlin

Introduction to Basic Science – Neuroimmunology


January  30th Michael Hoffmann, MD

University Eye Clinic, Otto von Guericke University, Madgeburg Germany

Electrophysiology of Visual Dysfunction

February  6th Marcus D’Souza, MD

Department of Neurology, University of Basel, Switzerland

Capturing disability in MS with kinect

February 13th Mir-Farzin Mashreghi, PhD

German Rheumatism Research Center, DRFZ, Berlin

The role of Regulatory RNA in Proinflammatory T-helper cells

February  20th


Véronique Blanchard, PhD

Institut für Labormedizin, Klinische Chemie und Pathobiochemie, Charité

The Glycome in Health and Disease





Neuroimmunological Colloquium @ AG Paul and NeuroCure/Charité Mitte

Dear Colleagues,

The next Neuroimmunological colloquium will take place on Monday, 30th January, 2017. This session will feature a talk by, Prof Dr. Michael Hoffmann from the University Eye Clinic, Otto von Guericke University, Magdeburg, Germany.

Topic: Electrophysiology of Visual Dysfunction


Venue: Campus Charité Mitte, Hufelandweg 6, Ferdinand Sauerbruch Hörsaal 4.

Time:  14:00


We provide continuing education credits by the Deutsche Ärztekammer and graduate student credits for Medical Neuroscience students.

Lunch and light drinks will be provided.

This year 2017 and for the rest of the Semester we have an exciting schedule of national and international presenters with expertise in diverse sub-areas of neuroimmunology.

Our hope is that this seminar will provide a platform to exchange ideas, create new collaborations, re-connect with colleagues and learn about the

novel research at the forefront of our neuroimmunology community.


Please feel free to forward the attached flyer to your colleagues and friends.


Looking forward to seeing you there!


Best regards,

Priscilla Koduah



Priscilla Koduah, PhD Candidate Neurodiagnostics Laboratory and Clinical Neuroimmunology Group NeuroCure Clinical Research Center Charité – Universitätsmedizin Berlin Charitéplatz 1 10117 Berlin, Germany Email:

Bremer et al. – Longitudinal Intravital Imaging of the Retina Reveals Long-term Dynamics of Immune Infiltration and Its Effects on the Glial Network in Experimental Autoimmune Uveoretinitis, without Evident Signs of Neuronal Dysfunction in the Ganglion Cell Layer

Front Immunol. 2016 Dec 23;7:642

by Bremer D, Pache F, Günther R, Hornow J, Andresen V, Leben R, Mothes R, Zimmermann H, Brandt AU, Paul F, Hauser AE, Radbruch H, Niesner R

(in cooperation with DRFZ AG Niesner)

A hallmark of autoimmune retinal inflammation is the infiltration of the retina with cells of the innate and adaptive immune system, leading to detachment of the retinal layers and even to complete loss of the retinal photoreceptor layer. As the only optical system in the organism, the eye enables non-invasive longitudinal imaging studies of these local autoimmune processes and of their effects on the target tissue. Moreover, as a window to the central nervous system (CNS), the eye also reflects general neuroinflammatory processes taking place at various sites within the CNS. Histological studies in murine neuroinflammatory models, such as experimental autoimmune uveoretinitis (EAU) and experimental autoimmune encephalomyelitis, indicate that immune infiltration is initialized by effector CD4+ T cells, with the innate compartment (neutrophils, macrophages, and monocytes) contributing crucially to tissue degeneration that occurs at later phases of the disease. However, how the immune attack is orchestrated by various immune cell subsets in the retina and how the latter interact with the target tissue under in vivo conditions is still poorly understood. Our study addresses this gap with a novel approach for intravital two-photon microscopy, which enabled us to repeatedly track CD4+ T cells and LysM phagocytes during the entire course of EAU and to identify a specific radial infiltration pattern of these cells within the inflamed retina, starting from the optic nerve head. In contrast, highly motile CX3CR+1 cells display an opposite radial motility pattern, toward the optic nerve head. These inflammatory processes induce modifications of the microglial network toward an activated morphology, especially around the optic nerve head and main retinal blood vessels, but do not affect the neurons within the ganglion cell layer. Thanks to the new technology, non-invasive correlation of clinical scores of CNS-related pathologies with immune infiltrate behavior and subsequent tissue dysfunction is now possible. Hence, the new approach paves the way for deeper insights into the pathology of neuroinflammatory processes on a cellular basis, over the entire disease course.