清除鼠肺囊虫感染不依赖于 MyD88。
Clearance of Pneumocystis murina infection is not dependent on MyD88.
机构信息
Critical Care Medicine Department, NIH Clinical Center, NIH, Building 10, Room 2C145, MSC 1662, Bethesda, MD 20892-1662, USA.
Laboratory of Immunopathogenesis and Bioinformatics, Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research, Frederick, MD 21702, USA.
出版信息
Microbes Infect. 2014 Jun;16(6):522-7. doi: 10.1016/j.micinf.2014.03.005. Epub 2014 Mar 25.
To determine if myeloid differentiation factor 88 (MyD88), which is necessary for signaling by most TLRs and IL-1Rs, is necessary for control of Pneumocystis infection, MyD88-deficient and wild-type mice were infected with Pneumocystis by exposure to infected seeder mice and were followed for up to 106 days. MyD88-deficient mice showed clearance of Pneumocystis and development of anti-Pneumocystis antibody responses with kinetics similar to wild-type mice. Based on expression levels of select genes, MyD88-deficient mice developed immune responses similar to wild-type mice. Thus, MyD88 and the upstream pathways that rely on MyD88 signaling are not required for control of Pneumocystis infection.
为了确定髓样分化因子 88（MyD88）是否对大多数 TLR 和 IL-1R 的信号转导是必需的，我们用感染有 Pneumocystis 的种子鼠感染 MyD88 缺陷型和野生型小鼠，并对其进行了长达 106 天的跟踪观察。MyD88 缺陷型小鼠清除了 Pneumocystis，产生了抗 Pneumocystis 的抗体反应，其动力学与野生型小鼠相似。基于选择基因的表达水平，MyD88 缺陷型小鼠产生了类似于野生型小鼠的免疫反应。因此，MyD88 和依赖于 MyD88 信号转导的上游途径对于控制 Pneumocystis 感染不是必需的。
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