{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,30]],"date-time":"2025-10-30T11:07:43Z","timestamp":1761822463472},"reference-count":44,"publisher":"American Society of Hematology","issue":"9","content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2001,5,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The CD95 receptor, a member of the tumor necrosis factor (TNF) receptor superfamily, mediates signals for cell death on specific ligand or antibody engagement. It was hypothesized that interferon \u03b1 (IFN-\u03b1) induces apoptosis through activation of the CD95-mediated pathway and that CD95 and ligands of the death domain may belong to the group of IFN-stimulated genes. Therefore, the effect of IFN-\u03b1 on CD95-CD95L expression, on the release of TNF-\u03b1, and on TNF receptor 1 expression in an IFN-sensitive human Burkitt lymphoma cell line (Daudi) was investigated. After 5 days' incubation, apoptosis in 81% of IFN-\u03b1\u2013treated Daudi cells was preceded by a release of TNF-\u03b1 and an induction of CD95 receptor expression. Although supernatants of IFN-treated Daudi cells induced apoptosis of CD95-sensitive Jurkat cells, CD95L was undetectable on protein or on messenger RNA levels, and the weak initial expression of TNF receptor 1 increased only slightly during IFN treatment. Surprisingly, binding of TNF-\u03b1 to CD95 was observed and confirmed by 3 different techniques\u2014enzyme-linked immunosorbent assay using immobilized CD95:Fc\u2013immunoglobulin G, immunoprecipitation assay using CD95 receptor precipitates of Daudi cells, and binding of sodium iodide 125\u2013TNF-\u03b1 to Daudi cells, which was strongly stimulated by IFN-\u03b1 and inhibited by CD95L, CD95:Fc, unlabeled TNF-\u03b1, and anti\u2013TNF-\u03b1 antibody. Preincubation of Daudi cells with antagonists of the CD95-mediated pathway resulted in an inhibition of IFN-\u03b1\u2013mediated cell death. The present investigation shows that IFN-\u03b1 induces autocrine cell suicide of Daudi cells by a cross-talk between the CD95 receptor and TNF-\u03b1. The CD95 receptor can be considered a third TNF receptor, in addition to p55 and p75.<\/jats:p>","DOI":"10.1182\/blood.v97.9.2791","type":"journal-article","created":{"date-parts":[[2002,7,27]],"date-time":"2002-07-27T12:46:47Z","timestamp":1027774007000},"page":"2791-2797","update-policy":"http:\/\/dx.doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":12,"title":["Autocrine cell suicide in a Burkitt lymphoma cell line (Daudi) induced by interferon \u03b1: involvement of tumor necrosis factor as ligand for the CD95 receptor"],"prefix":"10.1182","volume":"97","author":[{"given":"Heinz","family":"Gisslinger","sequence":"first","affiliation":[{"name":"From the Departments of Internal Medicine I and Nuclear Medicine and the Ludwig Boltzmann Institut for Experimental Endocrinology, University of Vienna, Austria; and the M.D. Anderson Cancer Center, University of Texas, Houston."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Razelle","family":"Kurzrock","sequence":"additional","affiliation":[{"name":"From the Departments of Internal Medicine I and Nuclear Medicine and the Ludwig Boltzmann Institut for Experimental Endocrinology, University of Vienna, Austria; and the M.D. Anderson Cancer Center, University of Texas, Houston."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Bettina","family":"Gisslinger","sequence":"additional","affiliation":[{"name":"From the Departments of Internal Medicine I and Nuclear Medicine and the Ludwig Boltzmann Institut for Experimental Endocrinology, University of Vienna, Austria; and the M.D. Anderson Cancer Center, University of Texas, Houston."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shuwei","family":"Jiang","sequence":"additional","affiliation":[{"name":"From the Departments of Internal Medicine I and Nuclear Medicine and the Ludwig Boltzmann Institut for Experimental Endocrinology, University of Vienna, Austria; and the M.D. Anderson Cancer Center, University of Texas, Houston."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shuren","family":"Li","sequence":"additional","affiliation":[{"name":"From the Departments of Internal Medicine I and Nuclear Medicine and the Ludwig Boltzmann Institut for Experimental Endocrinology, University of Vienna, Austria; and the M.D. Anderson Cancer Center, University of Texas, Houston."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Irene","family":"Virgolini","sequence":"additional","affiliation":[{"name":"From the Departments of Internal Medicine I and Nuclear Medicine and the Ludwig Boltzmann Institut for Experimental Endocrinology, University of Vienna, Austria; and the M.D. Anderson Cancer Center, University of Texas, 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