s one of the leading candidate triggers,’ said first author Jan Lünemann, a neurologist and immunologist at The Rockefeller University in New York. 'Epstein-Barr virus does not cause MS, but the immune response to this virus is different in MS patients, and our hypothesis is that the altered immune response contributes to the development and progression of the disease.'
The people with MS, who are universally infected with Epstein Barr virus, showed increased antibody responses to certain EBV proteins in previous studies, Lünemann said. 'Very recent investigations have shown that such enhanced responses occur years before onset of clinical symptoms of MS,' he noted, indicating that EBV plays an important role early in the development of the disease.
'Our aim was to investigate what causes these increased antibody concentrations and if T cell responses to EBV are different in patients with MS,' Lünemann said. He and Edwards focused on one viral protein, called Epstein-Barr virus-encoded nuclear antigen1 (EBNA1).
Epstein-Barr virus usually persists life-long inside immune system B cells and is kept under control by virus-specific T cells. When B cells divide, the virus produces EBNA1 and uses it to slip its own DNA into the new cell. T cells that target EBNA1 are a crucial component of EBV-specific immune responses in individuals without MS.
Lünemann, Edwards, and colleagues began by collecting T cells from 20 untreated patients with MS and 20 volunteers who had been infected by Epstein-Barr virus but did not have the autoimmune disease. They then isolated from each patient the T cells that specifically responded to EBNA1.
A series of experiments revealed a pattern among the EBNA1 T cells in MS patients that was not seen in the healthy volunteers. 'We saw a dual effect—not only was there an increased number of EBNA1 responsive T cells, but these T cells proliferated to a greater extent when they were stimulatPage: 1 2 3 4 Related medicine news :1
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