{"title":"MMD2的单等位基因突变导致常染色体显性侵袭性牙周炎。","authors":"Tomoyuki Iwata, Yoko Mizoguchi, Tetsuya Yoshimoto, Miyuki Tsumura, Fumiaki Sakura, Jeffrey R Johnson, Shinji Matsuda, Kazuhisa Ouhara, Yukiko Nagatani, Takaki Asano, Hidenori Ohnishi, Zenichiro Kato, Keichiro Mihara, Hirokazu Kanegane, Tomoya Ueda, Shinya Sasaki, Yuri Taniguchi, Yurika Ninomiya, Yoshinori Ohno, Kyoko Suzuki-Takedachi, Yusuke Sotomaru, Tetsushi Sakuma, Takashi Yamamoto, Yukiko Matsuda, Kodai Kume, Terukazu Sanui, Fusanori Nishimura, Mikihito Kajiya, Yasuyoshi Ueki, Hidemi Kurihara, Hiroyuki Morino, Satoshi Okada, Hideshi Kawakami, Noriyoshi Mizuno","doi":"10.1084/jem.20231911","DOIUrl":null,"url":null,"abstract":"<p><p>Aggressive periodontitis causes rapid destruction of periodontal tissue. It occurs at a young age with familial clustering. We report on the first time on molecular and cellular basis of a Mendelian form of autosomal dominant aggressive periodontitis. Monoallelic mutations in the monocyte to macrophage differentiation-associated 2 (MMD2) gene, encoding MMD2, in two Japanese families with autosomal dominant aggressive periodontitis are identified. Mutations, c.347 C>T (p.A116V) and c.377 G>C (p.R126P) in MMD2, disturbed fMLP-induced activation of Ras/ERK signaling. Additionally, abnormalities in the proteins of Golgi apparatus, a crucial contributor to innate immune signaling pathways, were identified in patients' neutrophils. The knock-in and knockout mice exhibited alveolar bone loss by ligature-induced periodontitis, along with impaired fMLP-induced chemotaxis, as found in the patients with MMD2 mutation. Our studies revealed that monoallelic mutations in MMD2 underlie the impairment of neutrophil chemotaxis, which leads to the development of autosomal dominant aggressive periodontitis.</p>","PeriodicalId":15760,"journal":{"name":"Journal of Experimental Medicine","volume":"222 9","pages":""},"PeriodicalIF":12.6000,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12262042/pdf/","citationCount":"0","resultStr":"{\"title\":\"Monoallelic mutations in MMD2 cause autosomal dominant aggressive periodontitis.\",\"authors\":\"Tomoyuki Iwata, Yoko Mizoguchi, Tetsuya Yoshimoto, Miyuki Tsumura, Fumiaki Sakura, Jeffrey R Johnson, Shinji Matsuda, Kazuhisa Ouhara, Yukiko Nagatani, Takaki Asano, Hidenori Ohnishi, Zenichiro Kato, Keichiro Mihara, Hirokazu Kanegane, Tomoya Ueda, Shinya Sasaki, Yuri Taniguchi, Yurika Ninomiya, Yoshinori Ohno, Kyoko Suzuki-Takedachi, Yusuke Sotomaru, Tetsushi Sakuma, Takashi Yamamoto, Yukiko Matsuda, Kodai Kume, Terukazu Sanui, Fusanori Nishimura, Mikihito Kajiya, Yasuyoshi Ueki, Hidemi Kurihara, Hiroyuki Morino, Satoshi Okada, Hideshi Kawakami, Noriyoshi Mizuno\",\"doi\":\"10.1084/jem.20231911\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Aggressive periodontitis causes rapid destruction of periodontal tissue. It occurs at a young age with familial clustering. We report on the first time on molecular and cellular basis of a Mendelian form of autosomal dominant aggressive periodontitis. Monoallelic mutations in the monocyte to macrophage differentiation-associated 2 (MMD2) gene, encoding MMD2, in two Japanese families with autosomal dominant aggressive periodontitis are identified. Mutations, c.347 C>T (p.A116V) and c.377 G>C (p.R126P) in MMD2, disturbed fMLP-induced activation of Ras/ERK signaling. Additionally, abnormalities in the proteins of Golgi apparatus, a crucial contributor to innate immune signaling pathways, were identified in patients' neutrophils. The knock-in and knockout mice exhibited alveolar bone loss by ligature-induced periodontitis, along with impaired fMLP-induced chemotaxis, as found in the patients with MMD2 mutation. Our studies revealed that monoallelic mutations in MMD2 underlie the impairment of neutrophil chemotaxis, which leads to the development of autosomal dominant aggressive periodontitis.</p>\",\"PeriodicalId\":15760,\"journal\":{\"name\":\"Journal of Experimental Medicine\",\"volume\":\"222 9\",\"pages\":\"\"},\"PeriodicalIF\":12.6000,\"publicationDate\":\"2025-09-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12262042/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Experimental Medicine\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1084/jem.20231911\",\"RegionNum\":1,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/7/15 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q1\",\"JCRName\":\"IMMUNOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Experimental Medicine","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1084/jem.20231911","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/7/15 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"IMMUNOLOGY","Score":null,"Total":0}
引用次数: 0
摘要
侵袭性牙周炎会迅速破坏牙周组织。它发生在年轻的家庭聚集性。我们首次报道孟德尔型常染色体显性侵袭性牙周炎的分子和细胞基础。在两个日本常染色体显性侵袭性牙周炎家族中发现了编码MMD2的单核细胞到巨噬细胞分化相关2 (MMD2)基因的单等位基因突变。突变,c.347C>T (p.A116V)和C .377g> C (p.R126P)在MMD2中,干扰了fmlp诱导的Ras/ERK信号的激活。此外,在患者的中性粒细胞中发现了高尔基体蛋白的异常,高尔基体是先天免疫信号通路的重要贡献者。在MMD2突变患者中发现,敲入和敲除小鼠表现出由结扎诱导的牙周炎引起的牙槽骨丢失,以及fmlp诱导的趋化性受损。我们的研究表明,MMD2的单等位基因突变是中性粒细胞趋化性损伤的基础,从而导致常染色体显性侵袭性牙周炎的发展。
Monoallelic mutations in MMD2 cause autosomal dominant aggressive periodontitis.
Aggressive periodontitis causes rapid destruction of periodontal tissue. It occurs at a young age with familial clustering. We report on the first time on molecular and cellular basis of a Mendelian form of autosomal dominant aggressive periodontitis. Monoallelic mutations in the monocyte to macrophage differentiation-associated 2 (MMD2) gene, encoding MMD2, in two Japanese families with autosomal dominant aggressive periodontitis are identified. Mutations, c.347 C>T (p.A116V) and c.377 G>C (p.R126P) in MMD2, disturbed fMLP-induced activation of Ras/ERK signaling. Additionally, abnormalities in the proteins of Golgi apparatus, a crucial contributor to innate immune signaling pathways, were identified in patients' neutrophils. The knock-in and knockout mice exhibited alveolar bone loss by ligature-induced periodontitis, along with impaired fMLP-induced chemotaxis, as found in the patients with MMD2 mutation. Our studies revealed that monoallelic mutations in MMD2 underlie the impairment of neutrophil chemotaxis, which leads to the development of autosomal dominant aggressive periodontitis.
期刊介绍:
Since its establishment in 1896, the Journal of Experimental Medicine (JEM) has steadfastly pursued the publication of enduring and exceptional studies in medical biology. In an era where numerous publishing groups are introducing specialized journals, we recognize the importance of offering a distinguished platform for studies that seamlessly integrate various disciplines within the pathogenesis field.
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