Blocking of adhesion molecules can reduce MS activity, but VLA-4 is not equally relevant for all immune cells; TH17 cells can enter the CNS without it, namely via MCAM expression. The MCAM phenotype will be analyzed, as well as its role in transmigration into the CNS, in immune surveillance under (non)inflammatory conditions, and its potential usage of integrin VLA-2, which is preferentially expressed by these cells. We will combine human and murine experiments using conventional approaches (kinase inhibitors, transgenic mice, EAE), but also state-of-the-art spinning-disc microscopy to visualize MCAM-mediated CNS infiltration in vivo.
| Schwab, Nicholas Christopher | Department for Neurology |
| Zarbock, Alexander | Clinic for Anaesthesiology, Surgical Critical Care Medicine and Pain Therapy |
| Schwab, Nicholas Christopher | Department for Neurology |
| Zarbock, Alexander | Clinic for Anaesthesiology, Surgical Critical Care Medicine and Pain Therapy |