Research press release


Nature Medicine

Removing the guesswork from multiple sclerosis


IFN-βは多発性硬化症の治療に広く使われているが、いつでも必ず効果があるわけではない。その理由はわかっていなかった。L Steinmanたちは、多発性硬化症のマウスモデルである実験的自己免疫性脳脊髄炎を研究し、IFN-βが治療で効果をあげられるかは、病気を引き起こした免疫細胞の種類に応じて決まることを発見した。症状の原因がいわゆるTH1細胞(ヘルパーT細胞の一種)の場合にはIFN-βが有効だったが、TH17細胞(別種のヘルパーT細胞)がかかわる場合にはIFN-βは病気を悪化させた。また重要な知見として、IFN-βに反応しない多発性硬化症患者は病気がかえって悪化すること、IFN-βに反応する患者に比べてTH17細胞が作るIL-17Fという分子を高レベルにもつことも判明した。


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.

doi: 10.1038/nm.2110


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