Clearance of Pneumocystis murina infection is not dependent on MyD88

被引：3
|
作者：
Ripamonti, Chiara [1 ]
Bishop, Lisa R. [1 ]
Yang, Jun [2 ]
Lempicki, Richard A. [2 ]
Kovacs, Joseph A. [1 ]
机构：
[1] NIH, Dept Crit Care Med, Ctr Clin, Bethesda, MD 20892 USA
[2] Frederick Natl Lab Canc Res, Leidos Biomed Res Inc, Lab Immunopathogenesis & Bioinformat, Frederick, MD 21702 USA
来源：
MICROBES AND INFECTION | 2014年 / 16卷 / 06期
基金：
美国国家卫生研究院;
关键词：
Pneumocystis; PCP; MyD88; Innate immunity; TLR; MACROPHAGE MANNOSE RECEPTOR; F-SP MURIS; HOST-DEFENSE; IN-VIVO; CRYPTOCOCCUS-NEOFORMANS; KNOCKOUT MICE; CARINII; TOLL-LIKE-RECEPTOR-2; TRANSMISSION; DEFICIENCY;
D O I：
10.1016/j.micinf.2014.03.005
中图分类号：
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号：
100102 ;
摘要：
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. Published by Elsevier Masson SAS on behalf of Institut Pasteur.
引用
收藏
页码：522 / 527
页数：6
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