Literature DB >> 15459302

Autoimmune lymphoproliferative syndrome with somatic Fas mutations.

Eliska Holzelova1, Cédric Vonarbourg, Marie-Claude Stolzenberg, Peter D Arkwright, Françoise Selz, Anne-Marie Prieur, Stéphane Blanche, Jirina Bartunkova, Etienne Vilmer, Alain Fischer, Françoise Le Deist, Frédéric Rieux-Laucat.   

Abstract

BACKGROUND: Impaired Fas-induced apoptosis of lymphocytes in vitro is a principal feature of the autoimmune lymphoproliferative syndrome (ALPS). We studied six children with ALPS whose lymphocytes had normal sensitivity to Fas-induced apoptosis in vitro.
METHODS: Susceptibility to Fas-mediated apoptosis and the Fas gene were analyzed in purified subgroups of T cells and other mononuclear cells from six patients with ALPS type III.
RESULTS: Heterozygous dominant Fas mutations were detected in the polyclonal double-negative T cells from all six patients. In two patients, these mutations were found in a fraction of CD4+ and CD8+ T cells, monocytes, and CD34+ hematopoietic precursors, but not in hair or mucosal epithelial cells.
CONCLUSIONS: Somatic heterozygous mutations of Fas can cause a sporadic form of ALPS by allowing lymphoid precursors to resist the normal process of cell death. Copyright 2004 Massachusetts Medical Society

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Year:  2004        PMID: 15459302     DOI: 10.1056/NEJMoa040036

Source DB:  PubMed          Journal:  N Engl J Med        ISSN: 0028-4793            Impact factor:   91.245


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