Publication date: Oct 08, 2019
Targeting the chemokine receptor CXCR6, a protein at the surface of a certain group of T helper cells, prevented the development of multiple sclerosis (MS) in a mouse model of the disease, a study reports. Immune CD4 positive T-cells, known as T helper cells, play an important role in the autoimmune reaction against myelin (the protective coat surrounding neurons), the hallmark of MS. These cells are characterized by high levels of two pro-inflammatory molecules, called IL1β and IL-23, that help to sustain the immune reaction. By using an antibody against CXCR6, the researchers were able to replicate their previous results, those showing that depleting Sb1-expressing T-cells halted the development of MS. -We’ve demonstrated in mice you can target these cells and get rid of them,” Eileen Remold-O’Donnell, PhD, of the Program in Cellular and Molecular Medicine at Boston Children’s Hospital, and the study’s senior author, said in a press release. They observed that samples of synovial fluid (joint liquid) from patients with inflammatory autoimmune arthritis had high levels of CXCR6-positive T helper cells, whereas peripheral blood samples had not. These findings -suggest that therapies to regulate Sb1 levels or, more realistically, strategies to deplete CXCR6-marked TH [T helper] cells hold promise for mitigating autoimmune disorders such as MS,” the study concluded.
|disease||MESH||experimental autoimmune encephalomyelitis|
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