{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T21:35:53Z","timestamp":1791063353348,"version":"4.1.0"},"reference-count":37,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2001,12,21]],"date-time":"2001-12-21T00:00:00Z","timestamp":1008892800000},"content-version":"vor","delay-in-days":323,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Immunology"],"published-print":{"date-parts":[[2001,2]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p>The cellular prion protein (PrP<jats:sup>c<\/jats:sup>) is a glycosyl\u2010phosphatidylinositol (GPI)\u2010linked cell surface protein, which is expressed at high density on nervous tissues and at lower levels on most other solid\u2010organ tissues. It is also expressed on peripheral blood mononuclear cells (PBMC) of all lineages. In lymphocytes, its level of expression is dependent upon the state of cell activation, and polyclonal anti\u2010PrP antisera partially block lectin\u2010induced T\u2010cell activation, suggesting a functional role of the protein in this process. Using the monoclonal antibody (mAb) 3F4 we examined PrP<jats:sup>c<\/jats:sup> surface immunoreactivity on leukaemic cell lines of T\u2010 and B\u2010cell origin, and unexpectedly observed a complete lack of PrP<jats:sup>c<\/jats:sup> cell\u2010surface expression in Daudi cells, while all other cell lines displayed discernible reactivity. We demonstrated the intracellular presence of PrP\u2010specific mRNA and PrP protein. The lack of surface PrP<jats:sup>c<\/jats:sup> is unrelated to the well\u2010known defect of \u03b2<jats:sub>2<\/jats:sub>\u2010microglobulin (\u03b2<jats:sub>2<\/jats:sub>m) expression in Daudi cells as other \u03b2<jats:sub>2<\/jats:sub>m\u2010deficient cells, such as the melanoma cell line F0\u20101 and spleen cells from \u03b2<jats:sub>2<\/jats:sub>m gene\u2010deleted mice, were not deficient in cell\u2010surface PrP<jats:sup>c<\/jats:sup>. Daudi cells failed to bind antibodies directed against all GPI\u2010linked cell surface proteins. In somatic hybridization experiments using murine spleen cells as partners, we observed <jats:italic>de novo<\/jats:italic> expression of human PrP<jats:sup>c<\/jats:sup>, CD55 and CD59, thus demonstrating in Daudi cells the availability of these gene products for GPI linkage and cell\u2010surface expression.<\/jats:p>","DOI":"10.1046\/j.1365-2567.2001.01166.x","type":"journal-article","created":{"date-parts":[[2003,3,12]],"date-time":"2003-03-12T02:27:59Z","timestamp":1047436079000},"page":"242-247","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["The failure of Daudi cells to express the cellular prion protein is caused by a lack of glycosyl\u2010phosphatidylinositol anchor formation"],"prefix":"10.1111","volume":"102","author":[{"given":"E.","family":"Morelon","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"V.","family":"Dodelet","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P.","family":"Lavery","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"N. 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