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Clearance of Pneumocystis murina infection is not dependent on MyD88
Institution:1. Critical Care Medicine Department, NIH Clinical Center, NIH, Building 10, Room 2C145, MSC 1662, Bethesda, MD 20892-1662, USA;2. Laboratory of Immunopathogenesis and Bioinformatics, Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research, Frederick, MD 21702, USA;1. Department of Biochemistry and Immunology, Institute of Biological Science, Federal University of Minas Gerais, MG, Brazil;2. Postgraduate Program in Health Sciences: Infectious Diseases and Tropical Medicine, Medical School, Federal University of Minas Gerais, Belo Horizonte, MG, Brazil;3. Department of General Biology, Institute of Biological Science, Federal University of Minas Gerais, MG, Brazil;4. Department of Pathology, Institute of Biological Science, Federal University of Minas Gerais, MG, Brazil;5. Department of Morphology, Institute of Biological Science, Federal University of Minas Gerais, MG, Brazil;6. Department of Microbiology, Institute of Biological Science, Federal University of Minas Gerais, MG, Brazil;7. Department of Pathology, Albert Einstein College of Medicine, Bronx, NY, USA;8. Department of Medicine, Albert Einstein College of Medicine, Bronx, NY, USA;9. Postgraduate Program in Biological Science, NUPEB, Federal University of Ouro Preto, Ouro Preto, MG, Brazil;1. Vaccine Research Center, University of Tampere Medical School, Biokatu 10, FI-33520 Tampere, Finland;2. Department of Pediatrics, Tampere University Hospital, Teiskontie 35, FI-33521 Tampere, Finland;1. School of Biomedical Sciences, CHIRI Biosciences Research Precinct, Faculty of Health Sciences, Curtin University, GPO Box U1987, Perth, Western Australia 6845, Australia;2. Department of Microbiology, Pathwest Laboratory Medicine WA, Queen Elizabeth II Medical Centre, Nedlands, Western Australia 6009, Australia;3. School of Medicine and Pharmacology, University of Western Australia, Crawley, Western Australia 6009, Australia;1. Grup d’Enginyeria Molecular, Institut Químic de Sarrià, Universitat Ramon Llull, Via Augusta 390, E-08017 Barcelona, Spain;2. Retrovirology Laboratory IrsiCaixa, Hospital Universitari Germans Trias i Pujol, Universitat Autònoma de Barcelona, 08916 Badalona, Spain
Abstract: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.
Keywords:PCP  MyD88  Innate immunity  TLR
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