A new study on the development of therapeutic monoclonal antibodies to treat neuroinflammatory and demyelinating disease entitled “SEMA4D compromises blood–brain barrier, activates microglia, and inhibits remyelination in neurodegenerative disease” was published in the journal Neurobiology of Disease by Ernest S. Smith part of Maurice Zauderer’s group from Vaccinex, Inc.
Vaccinex, Inc. is a private clinical-stage biotechnology company located in Rochester, New York, focused on the discovery and development of human therapeutic monoclonal antibodies as therapy against cancer and neurodegenerative diseases, such as multiple sclerosis and Huntington’s disease. The company uses their ActivMAb® Antibody Discovery Technology for quick, mammalian cell-based antibody selection using the rapid and sensitive virus panning selection and cell sorting to form its antibody collection.
Multiple sclerosis (MS) is defined by an immune-mediated demyelinating process, where damage of the protective covering (myelin sheath) of nerve fibers in the brain and spinal cord occurs, and is a neurodegenerative disease of the human central nervous system (CNS). Although MS pathogenesis is not clear, it seems that cerebral endothelial cells, which constitute the barrier that separates and protects the CNS from the peripheral circulation, play a crucial role in this process. Also, cerebral endothelial permeability, i.e. the flow of small molecules or immune cells in and out of the vessel into the CNS is altered in different clinical forms of MS. There is an urgent need to find new therapeutic targets and approaches to inhibit the development of MS. Semaphorin 4D (SEMA4D) triggers signaling cascades that induce glial activation, failure of the neuronal process, inhibition of the migration and differentiation of oligodendrocyte precursor cells (OPCs), and disruption of endothelial tight junctions that constitute the blood-brain barrier (BBB).
~~~~~~~~~~~~~~~~~~~~
.
.
.
Visit our MS Learning Channel on YouTube: http://www.youtube.com/msviewsandnews