巨噬细胞是HIV-1的靶细胞和主要储存细胞，在艾滋病致病机制中发挥重要作用。巨噬细胞的极化影响了HIV-1在细胞中的复制，其机制尚不清楚。LPS会刺激巨噬细胞发生极化而影响巨噬细胞功能，但是目前尚不清楚LPS诱导的巨噬细胞抗HIV-1活性与巨噬细胞的极化是否存在联系。我们前期研究验证了LPS对巨噬细胞的保护作用，发现LPS会使巨噬细胞进一步分化。由此我们假设：LPS通过使巨噬细胞发生极化而具有抑制HIV-1复制的能力，而TRIM5α则参与该极化过程。为了验证这一假设，本项目拟在前期研究基础上研究：LPS刺激下巨噬细胞的极化状态与HIV-1感染巨噬细胞的关系；TRIM5α在LPS诱导的极化状态与抗HIV-1活性中的作用。本研究将初步明确巨噬细胞极化与抗HIV-1活性的关系及TRIM5α在其中的作用机制，对于深入了解艾滋病的发病机制和病程进展具有重要的理论意义和潜在的应用价值。

Macrophage, which was target cell and major viral reservoirs of HIV-1, plays crucial roles in AIDS pathogenesis. Macrophage polarziation could influence HIV-1 replication, but its mechansim was not clear. LPS could influence macrophage's function by inducing polarization, however, it was not clear whether there was a relationship between anti-HIV-1 activity of macrophage induced by LPS and polarization. Our previous study proved that LPS could protect macrophage from HIV-1 infection and found that LPS induced macrophage differentiation. Therefore, we hypothesized that macrophage acquired anti-HIV-1 activity through polarizaiton induced by LPS and polarizaition was not independent of TRIM5α. In order to verify this hypothesis, we planed to study: the relationship between macrophage polarization induced by LPS and HIV-1 infection; the function of TRIM5α in polarization induced by LPS and anti-HIV-1 activity. Through this study, we hope to make sure the relationship between polarization and anti-HIV-1 activity and the mechanism of TRIM5α in macrophage polarization and anti-HIV-1 activity, which would hope to deepen the understanding about AIDS initation and development.