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| CMV IE-1 – Recombinant Protein |
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| Description |
CMV IE-1 Recombinant Protein is designed for the efficient loading of monocyte-derived dendritic cells (MoDCs) for the subsequent in vitro stimulation of IE-1-specific CD4+ and CD8+ T cells. The resulting secretion of effector cytokines permits the detection of IE-1-specific effector/memory T cells, for example, by MACS® Cytokine Secretion Assays, intracellular cytokine staining, or other technologies. Quantitative, phenotypical, or functional analysis of specific T cell immunity can provide important information on the natural course of immune responses in healthy or immunocompromised individuals. |
| Applications |
Background information Human cytomegalovirus (CMV, HCMV) is a member of the herpes virus group belonging to the subfamily of beta-herpes viruses. Between 50–85% of human adults are infected with CMV. Once infected, the virus persists in the organism. IN healthy organisms, infection is asymptomatic, but in immunocompromised patients CMV can cause severe diseases. CMV IE-1 (immediate early protein 1), also known as UL123, is a non-structural protein which is one of the first CMV antigens expressed in an infected cell, and predominantly induces a CD8+ T cell response. IE-1–specific T cells occur in infected individuals at frequencies comparable to those of pp65-specific CD8+ T cells.¹ Both CMV antigens, IE-1 and pp65, are considered to be dominant T cell targets. |
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| 106 human T cells from a CMV+ donor were restimulated for 6 hours using unloaded in vitro generated DCs or in vitro generated DCs loaded with CMV IE-1 – Recombinant Protein. After 2 hours of restimulation 1 μg/mL of brefeldin A was added. Cells were harvested, fixed, permeabilized, and IE-1–specific cells were intracellularly stained with Anti-IFN-γ-PE. T cells were counterstained with CD8-FITC. IFN-γ production of lymphocytes is shown. Cells were analyzed by flow cytometry using the MACSQuant® Analyzer. |
| Stimulated cells |
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| Unstimulated control |
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| Details |
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| References |
| 1. Kern, F. et al. (1999) J. Virol. 73: 8179–8184. |
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