The therapeutic efficacy of interferon-beta ― the major treatment for multiple sclerosis ― depends on what immune cell type is involved in the disease, according to a report in this week's Nature Medicine. The results suggest that MS patients who will benefit from IFN-beta treatment may be identifiable before therapy even begins.
Interferon-beta (IFN-beta) is widely used against multiple sclerosis but is not always effective, and the reasons for treatment failure are not understood. Lawrence Steinman and his colleagues studied experimental autoimmune encephalomyelitis ― the mouse version of multiple sclerosis ― and found that IFN-beta was successful therapeutically depending on the immune cell type that induced the disease. If symptoms were caused by so-called TH1 cells ― one type of immune system helpers ― IFN-beta worked, but if TH17 cells ― another type of immune system helpers ― were involved, IFN-beta made disease worse. Crucially, the team found that patients with multiple sclerosis who do not respond to IFN-beta had worse disease and higher levels of IL-17F, a molecule produced by TH17 cells, compared to responders.
These results raise the tantalizing possibility of identifying what patients will derive benefit from IFN-beta even before the treatment begins ― a prospect with important clinical and financial implications.