期刊
JOURNAL OF VIROLOGY
卷 79, 期 10, 页码 5943-5951出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.79.10.5943-5951.2005
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资金
- NIAID NIH HHS [AI13989, R01 AI013989, R37 AI013989] Funding Source: Medline
Previous studies have indicated that B cells make a significant contribution to the resolution of influenza virus infection. To determine how B cells participate in the control of the infection, we transferred intact, major histocompatibility complex class II (MHC-II) -negative or B-cell receptor (BCR)-transgenic spleen cells into B-celldeficient and CD8(+) T-cell-depleted mu MT mice, termed mu MT(-8), and tested them for ability to recover from infection. mu MT(-8) mice that received no spleen cells invariably succumbed to the infection within 20 days, indicating that CD4(+) T-cell activities had no significant therapeutic activity on their own; in fact, they were harmful and decreased survival time. Interestingly, however, they became beneficial in the presence of antiviral antibody (Ab). Injection of MHC-II((-/-)) spleen cells, which can provide CD4(+) T-cell-independent (TI) but not T-celldependent (TD) activities, delayed mortality but only rarely resulted in clearance of the infection. By contrast, 80% of mu MT(-8) mice injected with normal spleen cells survived and resolved the infection. Transfer of BCR-transgenic spleen cells, which contained similar to 10 times fewer virus-specific precursor B cells than normal spleen cells, had no significant impact on the course of the infection. Taken together, the results suggest that B cells contribute to the control of the infection mainly through production of virus-specific Abs and that the TI) Ab response is therapeutically more effective than the TI response. In addition, CD4(+) T cells appear to contribute, apart from promoting the TD Ab response, by improving the therapeutic activity of Ab-mediated effector mechanisms.
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