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  • Our results are consistent with the hypothesis that reduced

    2021-11-17

    Our results are consistent with the hypothesis that reduced Fas-mediated apoptosis in maternally activated T-lymphocytes could result in insufficient trophoblast invasion of the spiral such as as the activated T-lymphocytes become able to enhance the destruction of the cytotrophoblasts. A reduced number of invading cytotrophoblasts may lead to inadequate modification of the spiral arteries. This, in turn, predisposes to placental ischemia and vascular endothelial damage (Gerretsen et al., 1981, Roberts and Redman, 1993, Ness and Roberts, 1996).
    Conclusion The presence of the Fas gene polymorphism Fas A670G is associated with an increased risk of pre-eclampsia, while the presence of the FasLG IVS2nt 124 A>G gene may be protective against preeclampsia.
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    Conflict of interest
    Introduction Human adenoviruses (HAdVs) cause many types of illnesses, including various forms of respiratory, eye, and gastrointestinal disease (Wold and Isom, 2013). The strict species-specificity of adenoviruses complicates detailed studies of HAdV pathogenesis. We have established a mouse model of adenovirus respiratory infection using mouse adenovirus type 1 (MAV-1) to study the pathogenesis of an adenovirus in its natural host. MAV-1 replicates in lungs of mice following intranasal (i.n.) inoculation, with virus-induced inflammation, organ dysfunction, and dissemination to other organs that is reminiscent of disease seen in humans infected with HAdV (McCarthy et al., 2016, McCarthy et al., 2015a, McCarthy et al., 2014, Procario et al., 2012, Weinberg et al., 2005). CD8 T cell responses are important contributors to the control of many viral infections (Ehtisham et al., 1993, Kagi et al., 1994, Mullbacher et al., 1999, Schmidt and Varga, 2018, Walsh et al., 1994). HAdV-specific CD4 and CD8 T cells are detected in healthy adults (Hutnick et al., 2010). Patients with impaired cellular immune function are prone to more severe HAdV disease (Kojaoghlanian et al., 2003, Walls et al., 2003), indicating that T cell function is an important aspect of host defense against HAdV infection. T cells also serve as reservoirs for persistent infection in otherwise healthy individuals (Garnett et al., 2002, Garnett et al., 2009). Increased numbers of CD4 and CD8 T cells are detected in the lungs of mice during acute MAV-1 respiratory infection (McCarthy et al., 2015a, Procario et al., 2012, Weinberg et al., 2007), and CD8 T cells isolated from MAV-1-infected lungs produce effector molecules such as IFN-γ and granzyme B (GzmB) in a virus-specific manner (McCarthy et al., 2015b, McCarthy et al., 2014). Clearance of MAV-1 from the lungs is delayed in CD8 T cell-deficient mice (Molloy et al., 2017). CD8 T cell deficiency also inhibits MAV-1-induced airway inflammation and weight loss, indicating that CD8 T cells exert a pro-inflammatory effect that is independent of their effect on virus clearance. CD8 T cells recognize infected cells presenting virus-specific peptides via MHC class I. Subsequent CD8 T cell responses include production of pro-inflammatory cytokines such as IFN-γ, IL-2, and TNF-α; release of cytolytic granules containing perforin (Pfn) and granzyme B (GzmB); and the induction of apoptotic cell death via Pfn/GzmB-triggered pathways, interactions between Fas and Fas ligands (FasL), and interactions between tumor necrosis factor apoptosis-inducing ligand (TRAIL) and TRAIL receptors (Harty et al., 2000, Schmidt and Varga, 2018). The effects of CD8 T cells on virus clearance, virus-induced inflammation, and signs of disease during MAV-1 respiratory infection are largely independent of IFN-γ or Pfn (McCarthy et al., 2015b, Molloy et al., 2017). In this study, we sought to determine the extent to which another CD8 T cell effector pathway, interactions between FasL and Fas, mediated the antiviral and proinflammatory effects of CD8 T cells during acute MAV-1 respiratory infection.
    Methods and materials