B10

The formation and resolution of neuroinflammatory lesions is determined by the balance of lesion-inducing signals derived from infiltrating auto-reactive T cells and lesion-resolving signals at least in part derived from CNS resident cells. Here we now want to use CRISPR gene editing screens to characterize the molecular architecture underlying these critical neuro-immune interactions and validate the disease relevance of emerging communication pathways in deeply phenotyped bi-osamples from MS patients. In detail, we will tackle these questions:

1. 1. What are the molecular regulators that enable or limit CNS-entry of encephalitogenic T cells and how do they work?
   2. Which molecules contribute to the T-cell-instructed phagocyte recruitment and polarization?
   3. What kind of molecules contribute to the CNS-instructed phagocyte re-polarization?
      

      Locatelli et al., Nat Neurosci. 2018

Principal Investigators:

Univ.-Prof. Dr. med. Martin Kerschensteiner
Institut für Klinische Neuroimmunologie
München
martin.kerschensteiner@med.uni-muenchen.de

Priv.-Doz. Dr. rer. nat. Naoto Kawakami
Institut für Klinische Neuroimmunologie
München
naoto.kawakami@med.uni-muenchen.de