Citation Details
Pleiotropic defects in lymphocyte activation caused by caspase-8 mutations lead to human immunodeficiency
| Authors |  Chun HJ, Zheng L, Ahmad M, Wang J, Speirs CK, Siegel RM, Dale JK, Puck J, Davis J, Hall CG, Sgota-Smith S, Atkinson TP, Straus SE, Lenardo MJ |
| In | Nature (2002) 419: 395-399 |
| Genes of Interest | caspase-8 |
| Cells used in publication | T cell, unstim., human Human unstimulated T cells Blood/Immune Cells Primary Cells Species: human Tissue Origin: blood |
| Substrate | Plasmid (general) siRNA |
| Substrate Description | siRNA oligos GFP-fusion expressing plasmid antisense expressing plasmid |
| Applications | RNAiCo-Transfection |
| Topics | AntisenseApoptosisDiseases (e.g. HIV)Hereditary diseasesSignal transduction |
| Research Area | Immunology / Hematology |
| Relevant Products |  Human T Cell Nucleofector Kit |
| Vector Backbone | pEGFP |
Research Field
Caspase-8 is a member of the death-inducing signaling complex in apoptosis. Deficiency of caspase-8 causes defects in the activation of T lymphocytes, B lymphocytes and natural killer cells, which leads to immunodeficiency, suggesting that caspase-8 has a postnatal role in immune activation of naive lymphocytes.
Nucleofection Experiments
Peripheral blood T lymphocytes (PBLs) were transfected with caspase-8 RNAi.
In addition, PBLs were co-transfected with a caspase-8 antisense construct and a plasmid coding for eGFP.
Expression of caspase-8-GFP fusion protein in PBLs from a caspase-8 deficient patient rescued the impaired induction of the activation marker CD25 after stimulation.
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