PT -期刊文章盟Aurelien Parpaleix AU -瓦莱丽Amsellem盟Amal Houssaini AU -部门阿比德盟——Marielle Breau AU -伊丽莎白马科斯盟Daigo Sawaki AU -马里昂Delcroix盟Rozenn Quarck AU - Aurelie拉德盟Isabelle Couillin AU -伯纳德Ryffel盟哔叽Adnot TI -作用受体1 / MyD88信号在开发及肺动脉高压的发展援助- 10.1183/13993003.01448 -2015 DP - 2016年8月01 TA -欧洲呼吸杂志》第六PG - 470 - 483 - 48 IP - 2 4099 - //www.qdcxjkg.com/content/48/2/470.short 4100 - //www.qdcxjkg.com/content/48/2/470.full所以欧元和J2016 8月01;48 AB -肺动脉平滑肌细胞(PA-SMC)增殖和炎症肺动脉高血压(多环芳烃)的关键组件。白介素(IL) 1β与IL - 1受体结合(R) 1,从而招募分子适配器骨髓分化主要响应蛋白88 (MyD88)(参与IL-1R1和toll样受体信号转导)和诱导IL - 1、IL - 6,通过核factor-κB激活肿瘤坏死factor-α合成。我们调查了IL-1R1 / MyD88通路在肺动脉高压的发病机制。标记IL-1R1和MyD88表达式主要PA-SMC疣状被发现在特发性肺动脉高压患者的肺,小鼠低氧诱导肺动脉高压和SM22-5-HTT +老鼠。海拔在肺IL-1βIL-1R1 MyD88和il - 6之前在小鼠缺氧肺动脉高压。IL-1R1−−, MyD88−−和控制老鼠鉴于IL-1R1拮抗剂anakinra保护同样对缺氧性肺动脉高压和血管周的巨噬细胞招聘。Anakinra逆转肺动脉高压部分SM22-5-HTT +在monocrotaline-treated明显老鼠和老鼠。IL-1β-mediated鼠标PA-SMC增长的刺激是废除anakinra和缺席IL-1R1−−和MyD88−−老鼠。基因缺失局限于骨髓血统(M。lys-Cre MyD88fl / fl老鼠)降低肺动脉高压程度与控制,建议IL-1β-mediated PA-SMCs和巨噬细胞的影响。 The growth-promoting effect of media conditioned by M1 or M2 macrophages from M.lys-Cre MyD88fl/fl mice was attenuated.Pulmonary vessel remodelling and inflammation during pulmonary hypertension require IL-1R1/MyD88 signalling. Targeting the IL-1β/IL-1R1 pathway may hold promise for treating human PAH.The IL-1R1/MyD88 pathway is a treatment target for pulmonary arterial hypertension http://ow.ly/1Fpe3008RLs