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EBV Might Trigger Multiple Sclerosis, Study

ed by antigens,' said Edwards.

'We also examined T-cell responses to influenza hemagglutinin, antigens derived from cytomegalovirus, and even EBV antigens other than EBNA1,' Edwards said. 'The T-cell responses to these were all normal in MS patients, indicating a distinct role for EBNA1 in the disorder.'

The team then wanted to determine which portion of EBNA1 the T cells were recognizing. Generally, immune cells recognize one small, specific part on a protein, called an immunodominant region. Earlier evidence had pointed to one end of the protein, so the team decided to focus there. Münz supplied a series of 51 peptides—small segments of the EBNA1 protein—that the team added to T cells from MS patients and healthy controls.

As expected, the T cells in the healthy volunteers activated only in the presence of a specific group of peptides. But, Edwards said, 'EBNA1-specific T cells from the MS patients not only increased in frequency, but also recognized a much broader region of the protein, compared to healthy people who carried the EBV virus.' Immunologists call this phenomenon epitope-spreading. 'This was an interesting and unexpected finding,' said Edwards. 'At this point, I really believed we had a story.’

Finally, the team discovered that the hyper-reactive T cells belonged to the CD4 compartment of memory T cells and that these cells were strong producers of interferon-gamma, an anti-viral protein that shapes immune responses. 'Animal research has shown that pro-inflammatory CD4 cells directed against central nervous system antigens can trigger an MS-like disease,' said Edwards. 'So we knew we were looking at the right population of T cells.'

The next step will be to determine how these over-reactive immune cells trigger the destruction of the myelin sheathing that insulates nerve cells. 'The broadened response of the T cells could lead them to recognize and attack cells they aren't supposed to, like b
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