| First Author | Zhang C | Year | 2006 |
| Journal | Infect Immun | Volume | 74 |
| Issue | 3 | Pages | 1857-64 |
| PubMed ID | 16495560 | Mgi Jnum | J:107379 |
| Mgi Id | MGI:3621066 | Doi | 10.1128/IAI.74.3.1857-1864.2006 |
| Citation | Zhang C, et al. (2006) Toll-like receptor 2 mediates alveolar macrophage response to Pneumocystis murina. Infect Immun 74(3):1857-64 |
| abstractText | 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 murina organisms through Toll-like receptor 2 (TLR2), leading to the nuclear translocation of NF-kappaB 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-kappaB 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. murina. |
