{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T14:16:25Z","timestamp":1790864185219,"version":"4.1.0"},"reference-count":48,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2005,12,1]],"date-time":"2005-12-01T00:00:00Z","timestamp":1133395200000},"content-version":"vor","delay-in-days":4140,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Immunol"],"published-print":{"date-parts":[[1994,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>A critical event in B cell immortilization by Epstein\u2010Barr virus (EBV) is the establishment of an autocrine loop where cells produce a growth factor which supports their own proliferation. We investigated the potential of lymphoblastoid cell lines (LCL) and Burkitt lymphoma (BL) cell lines to produce and respond to the cytotoxins, tumor necrosis factor\u2010\u03b1 (TNF\u2010\u03b1) and lymphotoxin (LT). Transformation <jats:italic>in vitro<\/jats:italic> of peripheral blood B cells by EBV from seven different donors resulted in spontaneous production of both LT (11542 pg\/ml \u00b1 7546, mean \u00b1 SD) and, to a lesser extent, TNF\u2010\u03b1 (197 pg\/ml \u00b1 174). Similarly BL cell lines derived from <jats:italic>in vivo<\/jats:italic> transformation which developed a \u2018LCL\u2010like\u2019 phenotype <jats:italic>in vitro<\/jats:italic> (group III) produced more LT (1990 pg\/ml \u00b1 1740) than the \u2018group I\u2019 BL cell lines (&lt; 40 pg\/ml LT) which had maintained the original BL biopsy cell phenotype <jats:italic>in vitro.<\/jats:italic> Transformation of periphreal blood B cells to generate LCL also resulted in an increase in surface p75 (<jats:italic>p<\/jats:italic> &lt; 0.02) and to a lesser extent p55 (not significant, ns) TNF receptor (TNF\u2010R) expression. Similar increases in surface TNF\u2010R (p75 <jats:italic>p<\/jats:italic> &lt; 0.02, p55 ns) were observed on the \u2018group III\u2019 BL cell lines compared with the \u2018group I\u2019 BL cell lines. Proliferation of an LCL and a \u2018group III\u2019 BL cell line <jats:italic>in vitro<\/jats:italic> was via an autocrine loop since inhibition of LT reduced proliferation. This proliferation could also be blocked in the presence of the antagonistic anti\u2010p55 TNF\u2010R antibody, H398, but not the antagonistic antibody anti\u2010p75 TNF\u2010R antibody UTR\u20101. Furthermore, proliferation could be induced with the p55 agonistic antibody, HTR\u20109. In contrast to these observations with p55 TNF\u2010R antibodies, two out of six of the \u2018group III\u2019 BL lines (Jijoye and Oba) only expressed the p75 TNF\u2010R and proliferation of these cells could only be blocked by the antagonistic anti\u2010p75 TNF\u2010R antibody UTR\u20101. These data suggest that LT is an autocrine growth factor for lymphoblastoid cells, and BL cell lines which display an LCL phenotype. Furthermore, although both TNF\u2010R are increased on the surface of these cells, this autocrine growth signal is mediated principally through binding to the p55 TNF\u2010R.<\/jats:p>","DOI":"10.1002\/eji.1830240825","type":"journal-article","created":{"date-parts":[[2007,3,1]],"date-time":"2007-03-01T23:16:16Z","timestamp":1172790976000},"page":"1879-1885","source":"Crossref","is-referenced-by-count":32,"title":["Lymphotoxin acts as an autocrine growth factor for Epstein\u2010Barr virus\u2010transformed B cells and differentiated Burkitt lymphoma cell lines"],"prefix":"10.1002","volume":"24","author":[{"given":"Deena L.","family":"Gibbons","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Martin","family":"Roweu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrew P.","family":"Cope","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marc","family":"Feldmann","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fionula M.","family":"Brennan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2005,12]]},"reference":[{"key":"e_1_2_1_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/0167-5699(90)90098-T"},{"key":"e_1_2_1_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0065-230X(08)60886-6"},{"key":"e_1_2_1_4_2","first-page":"4562","volume":"43","author":"Blazer B. 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