{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,9,25]],"date-time":"2025-09-25T16:20:24Z","timestamp":1758817224035},"reference-count":30,"publisher":"Oxford University Press (OUP)","issue":"1","license":[{"start":{"date-parts":[[1991,1,1]],"date-time":"1991-01-01T00:00:00Z","timestamp":662688000000},"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":[[2008,6,28]]},"abstract":"<jats:title>SUMMARY<\/jats:title><jats:p>We studied the cellular function and lymphokine production of T cells from patients with X-linked lymphoproliferative disease (XLP) when activated by the challenge with Epstein-Barr virus (EBV) infection. We used an assay system in which T cells were stimulated with membrane antigens of autologous EBV-infected B lymphoblastoid cell lines (B-LCL) and we examined cellular and humoral factors derived from the stimulated T cells which control the growth of EBV-inlected B-LCL. Immunoglobulin secretion from the autologous B-LCL was suppressed with radiosensitive suppressor cells in the patients with XLP. The degree of suppression was correlated with the immunoglobulin levels in the serum of the patients with acquired hypogammaglobulinaemia (P&amp;lt;0.05). In addition, T cells from the patients with XLP failed to produce interferon-gamma (IFN-\u03b3) (P &amp;lt; 0.001). Moreover, the T cell supernatants from the patients with XLP were less potent to inhibit the B-LCL growth. This diminished inhibition of the B-LCL growth was correlated well with the decreased concentration of IFN-\u03b3 in the T cell supernatants. These findings suggest that suppressor cells may be activated in the patients with the hypogammaglobulinaemia phenotype of XLP. but the frequent development of B cell lymphoma in hypogammaglobulinaemia indicate that immunoglobulin suppression may not exert enough pressure on the in vivo growth of EBV-infected B cells. The defective secretion of IFN-\u03b3 may be, at least partially, responsible for the abnormal cytotoxic T cell and natural killer activities found in the patients with XLP, and may indicate the clinical evaluation about the preventive injection of IFN-\u03b3 against the development of malignant lymphoma.<\/jats:p>","DOI":"10.1111\/j.1365-2249.1991.tb05580.x","type":"journal-article","created":{"date-parts":[[2010,7,26]],"date-time":"2010-07-26T19:04:51Z","timestamp":1280171091000},"page":"10-16","source":"Crossref","is-referenced-by-count":15,"title":["Defective control of Epstein-Barr virus-infected B cell growth in patients with X-linked lymphoproliferative disease"],"prefix":"10.1093","volume":"83","author":[{"given":"N","family":"YASUDA","sequence":"first","affiliation":[{"name":"Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE, USA"}]},{"given":"P K","family":"LAI","sequence":"additional","affiliation":[{"name":"Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE, USA"},{"name":"Eppley Institute for Research in Cancer and Allied Disease, University of Nebraska Medical Center, Omaha, NE, USA"}]},{"given":"J","family":"ROGERS","sequence":"additional","affiliation":[{"name":"Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE, USA"}]},{"given":"D T","family":"PURTLO","sequence":"additional","affiliation":[{"name":"Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE, USA"},{"name":"Department of Pediatrics, University of Nebraska Medical Center, Omaha, NE, USA"},{"name":"Eppley Institute for Research in Cancer and Allied Disease, University of Nebraska Medical Center, Omaha, NE, USA"}]}],"member":"286","published-online":{"date-parts":[[2008,6,28]]},"reference":[{"key":"2022011709093439100_b1","doi-asserted-by":"crossref","first-page":"1","DOI":"10.1016\/0008-8749(86)90001-8","article-title":"Defective natural killing (NK) activity but retention of lymphocyte-mediated antibody-dependent cellular cytotoxicity (ADCC) in patients with X-linked lymphoproliferative syndrome (XLP)","volume":"100","author":"Argov","year":"1986","journal-title":"Cell Immunol"},{"issue":"Suppl. 97","key":"2022011709093439100_b2","first-page":"77","article-title":"Isolation of mononuclear cells and granulocytes from human blood. 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Immunol, Immunopathol."},{"key":"2022011709093439100_b19","doi-asserted-by":"crossref","first-page":"49","DOI":"10.1016\/0002-9343(82)90923-8","article-title":"Epstein-Barr virusinduced disease in males with the X-linked lymphoproliferative syndrome (XLP)","volume":"73","author":"Purtilo","year":"1982","journal-title":"Am. J. Med"},{"key":"2022011709093439100_b20","doi-asserted-by":"crossref","first-page":"935","DOI":"10.1016\/S0140-6736(75)92004-8","article-title":"X-linked recessive progressive combined variable immunodeficiency (Duncan's disease)","volume":"i","author":"Purtilo","year":"1975","journal-title":"Lancet"},{"key":"2022011709093439100_b21","doi-asserted-by":"crossref","first-page":"499","DOI":"10.1002\/ijc.2910110302","article-title":"Cellular localization of an Epstein-Barr virus (EBV)-associated complement fixing antigen in producer and non-producer lymphoblastoid cell lines","volume":"11","author":"Reedman","year":"1973","journal-title":"Int. J. 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