News

Mon, 09/03/2020
Breakthrough: SFB scientsists explain pathomechanism of Susac Syndrome
Münster. Neuroinflammation is often associated with blood-brain-barrier dysfunction, which contributes to neurological tissue damage. In a paper published in the renowned journal Nature Communications SFB 128 scientists from Mueenster reveal the pathophysiology of Susac syndrome (SuS), an enigmatic neuroinflammatory disease with central nervous system (CNS) endotheliopathy. By investigating immune cells from the blood, cerebrospinal fluid, […]...more
Wed, 04/03/2020
The brain is less immune-priviledged than we thought
Münster. Although the CNS is immune privileged, continuous search for pathogens and tumours by immune cells within the CNS is indispensable. Thus, distinct immune-cell populations also cross the blood–brain barrier independently of inflammation/under homeostatic conditions. It was previously shown that effector memory T cells populate healthy CNS parenchyma in humans and, independently, that CCR5-expressing lymphocytes […]...more
Mon, 27/01/2020
Featured Publication: Integrated single cell analysis of blood and cerebrospinal fluid leukocytes in multiple sclerosis
Münster. Cerebrospinal fluid (CSF) protects the central nervous system (CNS) and analyzing CSF aids the diagnosis of CNS diseases, but our understanding of CSF leukocytes remains superficial. Here, using single cell transcriptomics, SFB researchers identify a specific border-associated composition and transcriptome of CSF leukocytes. In an article published in Nature Communications, they show that multiple […]...more


Mon, 11/09/2017 | Prof. Stefan Bittner receives Hertie Foundation medMS MyLab Research Funding

Mainz. Prof. Stefan Bittner joins fellow SFB 128 researcher Klaus Lehmann-Horn as the second 2017 recipient of research funding from the Hertie Foundation within the „MyLab” framework. Prof. Stefan Bittner will be funded by the program medMS My Lab to execute a new multi-year research project whose goal is to examine new mechanisms involved in neuronal degeneration in multiple sclerosis. More . . .