{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,16]],"date-time":"2026-05-16T01:28:27Z","timestamp":1778894907717,"version":"3.51.4"},"reference-count":30,"publisher":"Oxford University Press (OUP)","issue":"1","license":[{"start":{"date-parts":[[2001,7,1]],"date-time":"2001-07-01T00:00:00Z","timestamp":993945600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2001,12,20]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p>CVI is a primary immunodeficiency characterized by a failure of B cell differentiation associated with an array of T cell defects, such as enhanced T cell apoptosis. In this study we investigated the mechanisms underlying CVI enhanced T cell death. We analysed both the expression of Fas using flow cytometry techniques and the expression of FasL mRNA using RT-PCR in CVI T cells. We could not find any significant differences between CVI and normal subjects with regard to Fas expression, although there was a subgroup of CVI patients with very high Fas expression which was accompanied by an up-regulation of FasL mRNA. However, attemps to induce Fas-mediated apoptosis in these high Fas expressing cells, as evaluated by propidium iodide staining and APO2\u00b77 staining, were unsuccessful. We also investigated intracellular levels of Bcl-2, bcl-xl and bax in CD4+ and CD8+\u2003CVI T cells, as well as the bax\/Bcl-2 ratio, using flow cytometry techniques but could not detect any differences between CVI and normal subjects. Finally we analysed TNF-RI and TNF-RII mRNA expression in CD4+ and CD8+\u2003CVI T cells using semiquantitative RT-PCR and found a significant increase in expression of both TNF-Rs in CD4+\u2003T cells from CVI patients. Our data suggest that the increased expression of both TNF-Rs on T cells may be one of the mechanisms responsible for the accelerated T cell apoptosis in CVI.<\/jats:p>","DOI":"10.1046\/j.1365-2249.2001.01560.x","type":"journal-article","created":{"date-parts":[[2003,3,11]],"date-time":"2003-03-11T10:27:07Z","timestamp":1047378427000},"page":"117-122","source":"Crossref","is-referenced-by-count":33,"title":["Enhanced T cell apoptosis in common variable immunodeficiency: negative role of the fas\/fasligand system and of the Bcl-2 family proteins and possible role of TNF-RS"],"prefix":"10.1093","volume":"125","author":[{"given":"M","family":"Di Renzo","sequence":"first","affiliation":[{"name":"Division of Clinical Immunology, The Mount Sinai Medical Center, 1425 Madison Avenue, New York City, New York, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"D","family":"Serrano","sequence":"additional","affiliation":[{"name":"Division of Clinical Immunology, The Mount Sinai Medical Center, 1425 Madison Avenue, New York City, New York, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Z","family":"Zhou","sequence":"additional","affiliation":[{"name":"Division of Clinical Immunology, The Mount Sinai Medical Center, 1425 Madison Avenue, New York City, New York, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"I","family":"George","sequence":"additional","affiliation":[{"name":"Division of Clinical Immunology, The Mount Sinai Medical Center, 1425 Madison Avenue, New York City, New York, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"K","family":"Becker","sequence":"additional","affiliation":[{"name":"Division of Clinical Immunology, The Mount Sinai Medical Center, 1425 Madison Avenue, New York City, New York, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"C","family":"Cunningham-Rundles","sequence":"additional","affiliation":[{"name":"Division of Clinical Immunology, The Mount 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