Regular ArticleNK Cell-Mediated Lysis of Autologous HCMV-Infected Skin Fibroblasts Is Highly Variable among NK Cell Clones and Polyclonal NK Cell Lines☆
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Suppression of NK cell-mediated cytotoxicity against PRRSV-infected porcine alveolar macrophages in vitro
2013, Veterinary MicrobiologyCitation Excerpt :For example, absence or down-regulation by infection or transformation of self-proteins that are normally expressed by host cells can elicit NK lytic activity (Vivier and Biron, 2002). The role of NK cells has been defined in a lot of virus infections such as influenza virus (Achdout et al., 2010), foot-and-mouth disease virus (Toka et al., 2009), herpes simplex virus (Thapa et al., 2008), ectromelia virus (Parker et al., 2007), murine and human cytomegalovirus (Arase et al., 2002; Carr et al., 2002), and human immunodeficiency virus (HIV) (Tomescu et al., 2007). In contrast, there is limited information on the NK cell response during PRRSV infection.
Expansion of CD94/NKG2C<sup>+</sup> NK cells in response to human cytomegalovirus-infected fibroblasts
2006, BloodCitation Excerpt :The proportions of dividing cells within each subset were calculated as described.39 CD94/NKG2C+ NK cell clones were tested in a 4-hour 51Cr-release assay against mock- and HCMV (Towne)-infected (24 or 72 hours) autologous or HFF fibroblasts,40 at different effector-target ratios. Cells were treated with Trypsin-EDTA (Invitrogen Gibco, Grand Island, NY) labeled with 51Cr and used in standard cytotoxicity assays.41
A high-efficiency system of natural killer cell cloning
2005, Journal of Immunological MethodsAssessing Anti-HCMV Cell Mediated Immune Responses in Transplant Recipients and Healthy Controls Using a Novel Functional Assay
2020, Frontiers in Cellular and Infection MicrobiologyRecurrent stimulation of natural killer cell clones with K562 expressing membrane-bound interleukin-21 affects their phenotype, interferon-γ production, and lifespan
2019, International Journal of Molecular Sciences
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This work was supported by NIH Grants AI24258 and CA49605 to P.P. W.H.C. was supported by the following grants: NIH Training Grant T32 AI07290-13,-14,-15 and the United Negro College Fund–Merck Science Initiative Fellowship and NIH K08 AI50779-01.
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To whom correspondence should be addressed at the Department of Structural Biology, Stanford University, Stanford, CA 94305-5126. Fax: (650) 723-8464. E-mail: [email protected].