A research group of the multiple sclerosis (MS) Center Amsterdam, led by assistant professor Gijs Kooij, studied the clinical potential of pro-resolving lipid mediator Lipoxin A4 in MS and model systems. They discovered that this lipid mediator not only ameliorated neuro-inflammation, but also that it dampened pro-inflammatory T cell responses in MS patient-derived cells. These results are now published in Cell Reports.
The development of drugs for brain diseases is difficult for several reasons. Unfortunately, the blood-brain barrier, which is there to prevent all kinds of undesirable substances from entering the brain, also causes important medicines to be stopped. In addition, animal models with which research is carried out mimic but limit the disease in patients.
The research by Elly Hol and Elga de Vries, called CONNECT, aims to develop a human cell model that is closer to the patient than current cell and animal models. They do this by using the latest technology from human stem cells to develop blood-brain barrier cells and link them to mini-brains.
More about the granting of a total of 5 million euros for research into human measurement models on the website :
In our previous paper we showed beneficial effects of targeting macrophage-specific Acly in the context of atherosclerosis. Here, we showed that despite a marked regulation of inflammatory responses in vitro, macrophage Acly deficiency does not translate into huge alterations in other acute and chronic inflammatory disorders in vivo.
Multiple sclerosis (MS) is the most common chronic neurodegenerative and neuroinflammatory disease in young adults and despite availability of many disease-modifying therapies most patients will eventually develop secondary progressive MS. Here, we uncovered two distinct MS-specific phenotypes of brain resident immune cells, microglia, that are driven by local meningeal inflammation and differentially associate with neuronal damage. Results suggest that these phenotypes may occur sequentially during chronic meningeal inflammation and that microglia lose their protective properties over time, leading to neuronal loss. Hence, timely targeting of the processes contributing to microglial activation in the progressive MS cortex provides an interesting therapeutic strategy to combat progressive MS.
In addition to general director professor Bernard Uitdehaag, professor Elga de Vries will join the newly established executive board as scientific director. Besides the two directors senior researchers from seven different departments where MS research is performed will form the general board of the MS Center Amsterdam.
Professor Bernard Uitdehaag, neurologist and chair of the department of Neurology at Amsterdam UMC, has been director of MS Center Amsterdam since 2013. From April 1, he will be joined for the daily management by professor Elga de Vries. She has been at Amsterdam UMC since 2000 as a neuro-immunological researcher in the department of Molecular Cell Biology and Immunology. Her research group Neuro-immunology focuses on unraveling disease mechanisms of MS at a cellular level in order to find new targets for treatments.
The general board consists of eight senior researchers from seven departments within Amsterdam UMC. Their task is to jointly provide the vision and mission of the MS Center Amsterdam and a draw a strategy to achieve set goals.
Members general board
· prof. dr. Jeroen Geurts, Anatomy and Neuroscience
· prof. dr. Vincent de Groot, Rehabilitation medicine
· prof. dr. Joep Killestein, Neurology
· prof. dr. Charlotte Teunissen, Clinical chemistry
· prof. dr. Bernard Uitdehaag, Neurology
· prof. dr. Paul van der Valk, Pathology
· dr. ir. Hugo Vrenken, Radiology and nuclear medicine
· prof. dr. Elga de Vries, Molecular Cell Biology and Immunology
MS Center Amsterdam Office
The managing and general board will be supported by the MS Center Amsterdam Office.
· dr. Annette van der Goes
· Karin Husken
5-year survival of 9% . The PDAC TME is characterized by dense fibrotic stroma
and suppressive immune cells that repress anti-tumor immune responses and
contribute to cancer progression. In this paper, Rodriguez et al showed that
pancreatic tumor cells present an increased expression of a particular glycan
structure, sialic acid, capable to shape immune responses by inducing
tolerogenic programs in myeloid cells. This work highlights a critical role for
sialylated glycans in controlling immune suppression and provides new potential
targets for cancer immunotherapy in PDAC.