Research press release


Nature Medicine

The immunology of epilepsy


脳の炎症はてんかんの重要な要因の1つだが、特定の炎症性分子がてんかんに与える影響については、完全には解明されていない。マウスの数種類のてんかんモデルを用いて、Annamaria Vezzaniたちは、HMGB1とよばれる分子がニューロンと神経膠から放出されることを発見した。このHMGB1が、病原体に対する免疫応答の主要な受容体の1つTLR4と結合して、発作を引き起こすこともわかった。


A signaling pathway known for its role in immune defense responses is also involved in epilepsy, according to a report in this week's Nature Medicine. The discovery could potentially be useful in the development of new anti-convulsant agents.

Brain inflammation is a major factor in epilepsy, but the impact of specific inflammatory molecules on the disease is not fully understood. Using several models of epilepsy in mice, Annamaria Vezzani and her colleagues discovered that release of a molecule called HMGB1 from neurons and glia and its interaction with a receptor key for the immune response against pathogens ― TLR4 ― promoted seizures.

The researchers also found that blocking the action of HMGB1 and TLR4 decreased seizure frequency. Mice lacking TLR4 were also resistant to manipulations known to induce seizures. Last, increased levels of HMGB1 and TLR4 in epileptogenic tissue from patients pointed to the potential human relevance of this mechanism, which could be targeted to develop new anticonvulsant agents.

doi: 10.1038/nm.2127


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