Assessment of aquaporin-4 (AQP4) antibody assays in European diagnostic centres

identified follicle-like structures containing B cells close to vessels and PDGFRb+ cells forming a reticular network expanding to the parenchyma. To find out if these structures could provide sufficient homing locations which support plasma cells to become long-lived, we performed 5-ethynyl-2′-deoxyuridine (EdU)-pulse experiments. During pulse, EdU is incorporated by dividing cells like plasma blasts. The detection of EdU-positive cells up to seven weeks after pulse suggests that niches in the CNS can favor survival of plasma cells. We then further analyzed the migration of plasma blasts to the CNS. Since the sphingosine-1-phosphate analogon FTY720 (fingolimod) is known to suppress immune cell trafficking, we performed EAE experiments under accompanying treatment with the drug. FTY720treated animals were resistant to EAE in contrast to control animals. Immunofluorescent histological findings confirmed that no immune cell infiltration took place in FTY720-treated animals and the protective effect of FTY720 was not due to retention of immune cells in spleen, lymph nodes or bone marrow, as proved by quantitative FACS analysis. Control mice displayed massive immune cell infiltration in the perivascular space and parenchyma of the CNS, some evidently of long-lived phenotype. These results can be useful to evaluate the therapeutic potential of targeting plasma cells in chronic neuroinflammation.