| First Author | Opata MM | Year | 2013 |
| Journal | Infect Immun | Volume | 81 |
| Issue | 11 | Pages | 4252-60 |
| PubMed ID | 24002064 | Mgi Jnum | J:201876 |
| Mgi Id | MGI:5516120 | Doi | 10.1128/IAI.00744-13 |
| Citation | Opata MM, et al. (2013) B Cell Production of Tumor Necrosis Factor in Response to Pneumocystis murina Infection in Mice. Infect Immun 81(11):4252-60 |
| abstractText | Pneumocystis species are opportunistic fungal pathogens that induce tumor necrosis factor (TNF) production by alveolar macrophages. Here we report that B cells from the draining lymph nodes as well as lung CD4(+) T cells are important producers of TNF upon Pneumocystis murina infection. To determine the importance of B cell-derived TNF in the primary response to P. murina, we generated bone marrow chimeras whose B cells were unable to produce TNF. The lung P. murina burden at 10 days postinfection in TNF knockout (TNFKO) chimeras was significantly higher than that in wild-type (WT) chimeras, which corresponded to reduced numbers of activated CD4(+) T cells in the lungs at this early time point. Furthermore, CD4(+) T cells isolated from P. murina-infected TNFKO chimeras were unable to stimulate clearance of P. murina upon adoptive transfer to recombinase-deficient (RAG1KO) hosts. Together, these data indicate that B cell-derived TNF plays an important function in promoting CD4(+) T cell expansion and production of TNF and facilitating protection against P. murina infection. |
