
<ArticleTitle>Decreased T cell stimulatory capacity of monocyte-derived human macrophages following herpes simplex virus type 1 infection.</ArticleTitle>
<AbstractText>Macrophages play a central role in establishing a specific immune response by acting as professional antigen presenting cells (APC) for T cells leading to a vigorous immune response. In order to analyze if Herpes simplex Virus (HSV) type 1 infection might affect the macrophage APC-function, monocyte-derived human macrophages were infected with HSV-1 strain F in vitro. Cocultures with allogeneic T cells revealed a strongly impaired stimulatory capacity of HSV-infected macrophages compared to uninfected controls which was not owing to a productive viral infection in macrophages. An increased expression of <prot><prot>Fas</prot> ligand</prot> (<prot>FasL</prot>/<prot>CD95L</prot>) was detected in HSV-infected macrophages by FACS analysis. Although the majority of the macrophages expressed high levels of <prot>Fas</prot> (<prot>CD95</prot>/<prot>Apo-1</prot>), the HSV-induced upregulation of <prot>FasL</prot> did not result in an increased autocrine apoptosis of macrophages which might be related to endogenous expression of the apoptosis inhibitor <prot>FLICE inhibitory protein</prot> (<prot>FLIP</prot>). However, substantial apoptosis occurred in peripheral T cells as well as <prot>Fas</prot>-sensitive Jurkat T cells when cocultured with HSV-infected macrophages. These findings suggest that the paracrine killing of activated T cells by <prot>FasL</prot> expressing APC might be a novel strategy of immune evasion by HSV.</AbstractText>
