Andrew N. Wilner, MD; Thomas P. Leist, MD

Disclosures

November 05, 2013

Editor's Note:
While onsite at the European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS) 2013 annual meeting in Copenhagen, Denmark, Medscape correspondent Andrew N. Wilner, MD spoke with Thomas P. Leist, Associate Professor of Neurology at Thomas Jefferson University in Philadelphia, Pennsylvania, about a promising therapeutic approach in multiple sclerosis (MS).

Autoimmunity in Multiple Sclerosis

Dr. Wilner: Dr. Leist, we have been hearing a lot about the immunopathology of MS, and the involvement of T cells is increasingly becoming a target of our therapies. Can you give us some background so that we can understand what is really happening with the disease and these treatments?

Dr. Leist: MS is an autoimmune disease like rheumatoid arthritis or psoriasis. Very often, we find that a patient with MS is at high risk of having a second autoimmune disease. Also, if we look at the families of patients with MS, in about 1 in 7 patients there is another relative with MS . Autoimmune diseases run in some families. Members of such families can have an up to 30% risk of having an autoimmune disorder such as MS.

From that point of view, we have a genetic contribution and an immune system dysregulation. The immune system is what protects us from the environment. In MS, the immune system changes from a purely protective mechanism to a mechanism that is also self-injurious. Most people have some evidence of autoimmunity (for example, antinuclear antibodies), but this doesn't lead to disease. The difference in MS is evidence of self-directed disease.

For a long time, primarily on the basis of animal experiments, it was thought that the T cells were the sole or the predominant cells causing disease. In recent years, we have used medications as a "reverse engineering process" of the disease state of MS. We use a medication and then turn around and ask how it works and what questions it answers. What new doors does this medication open for further investigation, particularly when the answer wasn't what we expected?

We recognized, initially on the basis of animal experiments that were then extended to humans, that CD4 cells play a role. We also learned in parallel that CD8 cells also contribute. B cells are also antigen-presenting cells. Their role is not just to produce antibodies; they also have a role in presenting the body with antigens to which the body should be reacting. For example, if we get our flu shot every year, the macrophages (the other cells of the antigen-presenting system) and the B cells present that vaccine and allow us to form an immune response.

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