High levels of a protein called calnexin in the brain may disrupt the blood-brain barrier of patients with multiple sclerosis, a Canadian study suggests.
The finding could lead to new treatment strategies to prevent brain damage in MS.
The research, “Calnexin is necessary for T cell transmigration into the central nervous system,” was published in the journal JCI Insight.
MS is an autoimmune disease regulated by the actions of white blood cells called T-cells in the brain and spinal cord. When activated, the cells cross the blood-brain barrier to cause inflammation and destroy myelin, which protects nerve fibers. These events lead to the progressive loss of cells and to the manifestations of MS.
Blood-brain barrier disruption is a hallmark of various disorders, including MS. When damaged, the shield no longer prevents the entry of certain cells and large molecules into the central nervous system, which may trigger inflammation and damage to neurons.
Calnexin is a protein found in a cell structure called endoplasmic reticulum (ER). In the ER, calnexin participates in the quality control of newly produced proteins.
In comparison with 10 healthy subjects, the investigators found unexpectedly high levels of calnexin in brain endothelial cells, which are key components of the blood-brain barrier.
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