Porphyromonas gingivalis Promotes Unrestrained Type I Interferon Production by Dysregulating TAM Signaling via MYD88 Degradation

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• 作者：Gabriel Mizrajip>1p>p> ; p>p>2p> ; Maria Nassarp>1p> ; Hadas Segevp>1p> ; Hafiz Sharawip>2p> ; Luba Eli-Berchoerp>1p> ; Tal Capuchap>1p> ; Tsipora Nirp>1p> ; Yaara Tabibp>1p> ; Avraham Maimonp>1p> ; Shira Dishonp>1p> ; Lior Shapirap>2p> ; Gabriel Nussbaump>1p> ; Asaf Wilenskyp>2p>p> ; p>p>asafw@ekmd.huji.ac.ilp> ; Avi-Hai Hovavp>1p>p> ; p>p>3p>p> ; p>p>avihaih@ekmd.huji.ac.ilp>
• 关键词：oral mucosa ; mucosal immunity ; periodontitis ; Porphyromonas gingivalis ; MYD88 ; interferon ; GAS6
• 刊名：Cell Reports
• 出版年：2017
• 出版时间：10 January 2017
• 年：2017
• 卷：18
• 期：2
• 页码：419-431
• 全文大小：3872 K
• 卷排序：18

文摘

Type I interferons are upregulated in P. gingivalis-induced periodontitis in mice P. gingivalis causes degradation of MYD88 in the gingival epithelium MYD88 is required for AXL and GAS6 expression, regulators of type I interferons Blocking type I interferon signaling prevents experimental periodontitis