{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,3]],"date-time":"2026-02-03T01:35:06Z","timestamp":1770082506189,"version":"3.49.0"},"reference-count":62,"publisher":"Oxford University Press (OUP)","issue":"8","license":[{"start":{"date-parts":[[2001,4,1]],"date-time":"2001-04-01T00:00:00Z","timestamp":986083200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2001,4,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>In early CD4\u2212CD8\u2212 pro-thymocytes, signaling through the pre-TCR is crucial for survival and differentiation into CD4+CD8+ cells. At this more mature stage, interactions between \u03b1\u03b2TCR and self-Ag\/MHC complexes in turn lead either to cell survival and differentiation (positive selection) or to cell death (negative selection). Intrinsic differences must therefore exist between pre-TCR signals in CD4\u2212CD8\u2212 thymocytes and \u03b1\u03b2TCR signals in CD4+CD8+ cells, since only the latter can mediate a death signal. In this work, we directly compared the capability of pre-TCR and \u03b1\u03b2TCR to induce apoptosis in a CD4\u2212CD8\u2212 thymoma cell line following receptor cross-linking with mAbs. Cross-linking of \u03b1\u03b2TCR triggered high levels of programmed cell death, mimicking the negative selection signal usually induced in CD4+CD8+ thymocytes. In contrast, pre-TCR was very inefficient at inducing apoptosis upon cross-linking, despite similar levels of surface receptor expression. Importantly, inefficient apoptosis induction by the pre-TCR did not result from its weak association with TCR\u03b6 chain, since TCRs containing \u03b1-pT\u03b1 chimeric chains, binding weakly to TCR\u03b6, were still able to induce apoptosis. Although similar tyrosine phosphorylation and calcium influx were induced after either pre-TCR or \u03b1\u03b2TCR cross-linking, the two pathways diverged at the level of Fas ligand induction. Among putative transcription factors involved in Fas ligand mRNA induction, Nur77 and NFAT transcriptional activities were readily induced after \u03b1\u03b2TCR, but not pre-TCR, stimulation. Together, these results support the view that the structure of the pre-TCR and \u03b1\u03b2TCR directly influences their apoptosis-inducing capabilities by activating distinct signaling pathways.<\/jats:p>","DOI":"10.4049\/jimmunol.166.8.5044","type":"journal-article","created":{"date-parts":[[2014,4,20]],"date-time":"2014-04-20T21:57:27Z","timestamp":1398031047000},"page":"5044-5050","source":"Crossref","is-referenced-by-count":10,"title":["Opposite Ability of Pre-TCR and \u03b1\u03b2TCR to Induce Apoptosis"],"prefix":"10.1093","volume":"166","author":[{"given":"Ann-Muriel","family":"Steff","sequence":"first","affiliation":[{"name":"Division of Research and Development, PROCREA BioSciences , Montreal, Quebec ,","place":["Canada"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Se\u0301bastien","family":"Trop","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Experimental Medicine, McGill University , Montreal, Quebec ,","place":["Canada"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mario","family":"Maira","sequence":"additional","affiliation":[{"name":"Institut de Recherches Cliniques de Montre\u0301al , Montreal, Quebec ,","place":["Canada"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jacques","family":"Drouin","sequence":"additional","affiliation":[{"name":"Institut de Recherches Cliniques de Montre\u0301al , Montreal, Quebec ,","place":["Canada"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Patrice","family":"Hugo","sequence":"additional","affiliation":[{"name":"Division of Research and Development, PROCREA BioSciences , Montreal, Quebec ,","place":["Canada"]},{"name":"Department of Medicine, Division of Experimental Medicine, McGill University , Montreal, Quebec ,","place":["Canada"]}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2001,4,15]]},"reference":[{"key":"2026020209162553300_R1","first-page":"433","volume-title":"Annu. 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