Targeting T cells is an effective target for blocking multiple sclerosis in an animal model of disease, according to researchers at Wayne State University’s School of Medicine. They believe that their study puts an end to the debate over whether or not T cells involved in each relapse were different and thus not suitable targets for therapy.
“It was important to resolve this issue because the two models suggested totally different therapeutic approaches,” remarks Harley Tse, Ph.D., associate professor of immunology and microbiology. Dr. Tse’s study was published in the January edition of the Journal of Neuroimmunology. The paper is titled “T cells that trigger acute experimental autoimmune encephalomyelitis also mediate subsequent disease relapses and predominantly produce IL-17.”
The conflicting conjectures in the research community were centered on treatment of the most common form of the disease, the remitting-relapse form. “Scientists have been trying to understand how and why the relapse cycles occur and to design therapy to delay disease relapses and hence prolong the remission period,” Dr. Tse notes. Some investigators found that the T cells involved in each relapse were directed against different myelin proteins. Others, however, could not find support for this in their studies.
To study the possibilities, Dr. Tse constructed a special mouse strain to tag the disease-causing T cells. He observed that when these marked T cells were eliminated after a relapse, subsequent relapses did not occur.
“Elimination of marked donor T cells could be done after development of the second or the third relapse episodes and each time, no further relapses occurred,” Dr. Tse explains. “This work is significant because for the first time we are able to definitively establish a cause-and-effect relationship linking the marked T cells to the development of relapses and show unambiguously that it was the same T cells that mediated relapsing cycles.”