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副作用の少ない、新しいアトピー性皮膚炎の治療薬の開発につながるか――。
皮膚をバリアーし保護するタンパク質の働きを強める化合物を京都大のチームが発見、この物質を使ってマウスのアトピー性皮膚炎の症状を改善させることに成功し、9月16日付の米科学誌電子版に発表した。47NEWSが伝えた。
時事ドットコムによると、アトピー性皮膚炎は、皮膚の保護機能が低下することで異物の混入を招き、免疫異常が起きて発症する。皮膚の保護では「フィラグリン」と呼ばれるたんぱく質が重要な働きをしていることが知られており、アトピー性皮膚炎のほぼ全ての患者でフィラグリンが低下している。
フィラグリンは皮膚のバリア機能に必須の蛋白です。アトピー性皮膚炎は、多様な病因、増悪因子が絡んで発症しますが、フィラグリン遺伝子変異は現在知られているアトピー性皮膚炎の発症因子の中で、最も頻度の高い因子です。
(名古屋大学医学部皮膚科「アトピー性皮膚炎の発症因子・フィラグリン遺伝子変異」より)
チームによると、アトピー性皮膚炎の治療には炎症を抑える外用薬などがあるが、皮膚が薄くなったり病原体に感染しやすくなったりする副作用が出ることがある。今回の化合物はアレルゲンになる物質を皮膚に取り込まないよう作用する。新たな治療薬となる可能性があり、10年後をめどに実用化を目指す。
京都大学大学院医学研究科の椛島健治准教授は、「保湿効果があるフィラグリンを増やす物質を見つけることは、世界中で競争になっていた。成果を基に薬の開発につなげたい」と話している。
アトピー性皮膚炎の研究をめぐっては、兵庫医科大学と三重大学のチームが8月6日、皮膚などにあるタンパク質「インターロイキン33」(IL33)が発症のメカニズムを解明したことを発表している。アトピー性皮膚炎に悩む人々にとって、さらなる研究の進展が望まれる。
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