Analysis for the pathogenesis of concomitant infection in AIDS and murine AIDS

LP-BM 5骨髓瘤病毒（MuLV）注射是一种导致的骨髓瘤艾滋病（MAIDS），由免疫细胞的功能异常和各种感染的可持续性表征。Bovis BCG是由生存率和细菌计数评估的。在PeritoneMacrophes中IL-15的表达在MAIDS中严重受到影响，导致M.。bovis BCG。NK细胞在卡介苗感染后的早期阶段中增加了正常老鼠的周穴，当这种增加在MAIDS老鼠中没有发现。血清IFN-γ水平也被抑制在卡介苗感染后的MAIDS老鼠。生产IFN-T细胞的γ-T细胞从M.感染的MAIDS老鼠Bovis BCG对PPD的反应明显较低，因为它被M.感染了正常的老鼠。bovis BCG。这些结果建议在MAIDS中抑制IL-15的生产可能会在针对M.的可疑性下被抑制。Bovis BCG.为了在MAIDS的进展中利用IL-15的保护作用，我们将IL-15 cDNA构建在MHC I类启动子下的转基因老鼠控制下。IL-15 Tg mice constitutionally produced a significant level of IL-15 protein and had markedly increased numbers of memory type （CD44型D1 high型D1 Ly6C型D1+型D1） of CD8型D1+型D1T cells in the LN。这些mice showed res\to LP-BM 5 infection accompanied by increases in NK cells and memory CD8--D1+ D1T cells and enh\IFN-production。因此，这些发现建议IL-15的生产对MAIDS的进展有一定的影响，IL-15可能对MAIDS和艾滋病的进展起到保护作用。

LP-BM5 murine leukemia virus (MuLV) injection is a causative of murine AIDS (MAIDS), characterized by a variety of functional abnormalities of immunocompetent cells and susceptibility to various infectious with Mycobacterium avium or M. bovis BCG as assessed by survival rate and bacterial counts. The expression of IL-15 in the peritoneal macrophages was severely impaired in MAIDS mice following infection with M. bovis BCG. NK cells were increased in the peritoneal cavity of normal mice at earl stage after BCG infection, whereas such increases were not evident in MAIDS mice. Serum IFN-γ level was also depressed in MAIDS mice following BCG infection. The production IFN-γ by T cells from the MAIDS mice infected with M. bovis BCG was significantly lower in response to PPD than that of normal mice infected with M. bovis BCG. These results suggested that depressed IL-15 production in MAIDS mice might be involved in susceptibility against M. bovis BCG.To elucidate the protective roles of IL-15 in the progression of MAIDS, we constructed transgenic mice using IL-15 cDNA under the control of an MHC class I promoter. The IL-15 Tg mice constitutionally produced a significant level of IL-15 protein and had markedly increased numbers of memory type (CD44ィイD1highィエD1 Ly6CィイD1+ィエD1) of CD8ィイD1+ィエD1T cells in the LN. These mice showed resistance to LP-BM5 infection accompanied by increases in NK cells and memory CD8ィイD1+ィエD1 T cells and enhanced IFN-γ production. Thus, these findings suggest that IL-15 production is partly responsible for MAIDS progression and that IL-15 may be protective for MAIDS and presumably AIDS progression.