期刊
INFECTION AND IMMUNITY
卷 74, 期 3, 页码 1857-1864出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/IAI.74.3.1857-1864.2006
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资金
- NHLBI NIH HHS [R01 HL065170, R01 HL65170] Funding Source: Medline
The innate immune response to Pneumocystis infection is not well understood. In this study, normal C57BL/6 mouse alveolar macrophages were found to respond to Pneumocystis marina organisms through Toll-like receptor 2 (TLR2), leading to the nuclear translocation of NF-kappa B and the production of proinflammatory cytokine tumor necrosis factor alpha (TNF-alpha) and chemokine macrophage inflammatory protein 2 (MIP-2). P. murina stimulation of normal alveolar macrophages from C57BL/6 mice resulted in increased TLR2 transcription but not increased TLR4 transcription. In gain-of-function studies with HEK293 cells expressing TLR2 or TLR4, only TLR2 was found to stimulate an NF-kappa B response to P. murina. TNF-alpha and MIP-2 production in response to P. murina by mouse alveolar macrophages was inhibited by a monoclonal antibody that specifically blocked the ligand-binding ability of TLR2. Alveolar macrophages from TLR2 knockout (TLR2(-/-)) mice showed little increase in TNF-alpha and MIP-2 mRNA levels upon P. murina stimulation. An in vivo study showed that TLR2(-/-) mice challenged with P. murina had reduced cytokine responses. These results indicate that TLR2 plays a major role in the innate immune response to P. marina.
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