Multiple sclerosis (MS) is a chronic inflammatory autoimmune disease of the central nervous system (CNS) resulting from a breakdown in peripheral immune tolerance. Although a beneficial role of natural killer (NK)-cell immune-regulatory function has been proposed, it still needs to be elucidated whether NK cells are functionally impaired as part of the disease. We observed NK cells in active MS lesions in close proximity to T cells. In accordance with a higher migratory capacity across the blood-brain barrier, CD56

Our findings provide a detailed characterization of different MDSC subsets in GBM patients and indicate that both granulocytic MDSCs in peripheral blood and at the tumor site play a major role in GBM-induced T-cell suppression.

Schneider-Hohendorf describe expression of adhesion molecules MCAM and PSGL-1 on human CD4+ T cells and Th17 T cells in multiple sclerosis patients under long-term natalizumab treatment. The authors identify that despite blockade of VLA-4, MCAM+ T cells can migrate through the blood–brain barrier to access the CNS through PSGL-1 and MCAM.

The cell-based assessment of the percentage of l-selectin-expressing CD4 T cells could provide an urgently needed biomarker for individual PML risk assessment.