News

Tue, 08/09/2020
Study with identical twins shows that the early form of multiple sclerosis has a specific pattern
The tremendous heterogeneity of the human population presents a major obstacle in understanding how autoimmune diseases like multiple sclerosis (MS) contribute to variations in human peripheral immune signatures. To minimize heterogeneity, SFB researchers from Munich and Muenster made use of a unique cohort of 43 monozygotic twin pairs clinically discordant for MS and searched for […]...more
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, 09/03/2020 | Breakthrough: SFB scientsists explain pathomechanism of Susac Syndrome

SFB researchers Dr. Catharina Groß, Prof. Dr. Heinz Wiendl and their team have deciphered important processes in Susac syndrome (Photo: UKM-Fotozentrale / Monecke)

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, and CNS of SuS patients, Dr. Catharina Gross and her team demonstrate oligoclonal expansion of terminally differentiated activated cytotoxic CD8+ T cells (CTLs). Neuropathological data derived from both SuS patients and a newly-developed transgenic mouse model recapitulating the disease indicate that CTLs adhere to CNS microvessels in distinct areas and polarize granzyme B, which most likely results in the observed endothelial cell injury and microhemorrhages. The autors show that blocking T-cell adhesion by anti-α4 integrin-intervention ameliorates the disease in the preclinical model. Similarly, disease severity decreases in four SuS patients treated with natalizumab along with other therapy. Their study identifies CD8+ T-cell-mediated endotheliopathy as a key disease mechanism in SuS and highlights therapeutic opportunities.

Adapted from: Gross CC, Meyer C, Bhatia U, Yshii L, Kleffner I, Bauer J, Tröscher AR, Schulte-Mecklenbeck A, Herich S, Schneider-Hohendorf T, Plate H, Kuhlmann T, Schwaninger M, Brück W, Pawlitzki M, Laplaud DA, Loussouarn D, Parratt J, Barnett M, Buckland ME, Hardy TA, Reddel SW, Ringelstein M, Dörr J, Wildemann B, Kraemer M, Lassmann H, Höftberger R, Beltrán E, Dornmair K, Schwab N, Klotz L, Meuth SG, Martin-Blondel G, Wiendl H, Liblau R. CD8+ T cell-mediated endotheliopathy is a targetable mechanism of neuro-inflammation in Susac syndrome. Nat Commun. 2019 Dec 18;10(1):5779.