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Scientists
have long known that the central nervous system (CNS) has a remarkable ability
to limit excessive inflammation in the presence of antigens or injury, but how
it works has been unclear. Now, Yale researchers have identified a mechanism
that offers this new insight into this protective effect. The findings were
described in the April 8 journal of Science Advances.
Until
now, the prevailing theory has been that the blood brain barrier provided the protective effect by preventing immune
cells and molecules from entering the brain. However, when
inflammation does occur, the brain has a way other than the blood brain barrier
of slowing or stopping it, the Yale team observed.
Just
as humans communicate using language, cells communicate using cell surface
molecules and soluble proteins. And it is a particular conversation between a
protein known as HVEM (herpes virus entry mediator) and SALM5, a molecule
mainly found in neuronal cells, that suppresses CNS inflammation, said senior
author on the paper, Lieping Chen, MD, PhD United Technologies Corporation
Professor in Cancer Research, professor of immunobiology, dermatology, and
medicine (medical oncology); and co-director, cancer immunology program at Yale
Cancer Center.
"We've
identified a key molecular pathway that may control CNS inflammation and
provide evidence that this pathway could be manipulated by a monoclonal
antibody to enhance immune response," Chen said. "Also, we
developed a new receptor array technology to identify the interaction between
HVEM and SALM5. Both discoveries could be applied to the study of other
pathways in the search for new therapies."
Chen
said his team's interpretation opens the way for new drugs that can control CNS
disease, including brain tumors. Specifically, using a strategy similar the
anti-PD1/anti-PDL1 therapy developed in his lab many years ago to promote
immune response in other human cancers.
http://medicalxpress.com/news/2016-04-central-nervous-inflammationa-pathway-drug.html
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