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Prepublished online as a Blood First Edition Paper on May 15, 2003; DOI 10.1182/blood-2003-01-0114. This Article Full Text Full Text (PDF) All Versions of this Article: 2003-01-0114v1 102/6/2053    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Dufour, C. Articles by Pistoia, V. Search for Related Content PubMed PubMed Citation Articles by Dufour, C. Articles by Pistoia, V. Related Collections Hematopoiesis and Stem Cells Immunobiology Red Cells Chemokines, Cytokines, and Interleukins Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 15 September 2003, Vol. 102, No. 6, pp. 2053-2059 HEMATOPOIESIS TNF- and IFN- are overexpressed in the bone marrow of Fanconi anemia patients and TNF- suppresses erythropoiesis in vitro Carlo Dufour, Anna Corcione, Johanna Svahn, Riccardo Haupt, Vincenzo Poggi, Albert Nandor Béka'ssy, Rosanna Scimè, Angela Pistorio, and Vito Pistoia From the Hematology Unit, Department of Pediatric Hemato-Oncology, G. Gaslini Children's Hospital, Genova, Italy; Laboratory of Oncology, G. Gaslini Children's Hospital, Genova, Italy; Epidemiology and Biostatistics Section, Scientific Directorate, G. Gaslini Children's Hospital, Genova, Italy; Pediatric Hematology Unit, Pausillipon Hospital, Napoli, Italy; University Hospital Lund, Department of Pediatric Hematology-Oncology, Lund, Sweden; and Department of Hematology and BMT Unit, V. Cervello Hospital, Palermo, Italy. In Fanconi anemia (FA) C mice tumor necrosis factor (TNF-) and interferon (IFN-) have key roles in the pathogenesis of bone marrow failure. In FA subjects TNF- was found to be increased in the serum and overproduced by patient-derived B-cell lines. In acquired aplastic anemia, a disease in which, similarly to FA, marrow failure occurs, TNF- and IFN- act as late mediators of the stem cell damage and are overexpressed in patient marrow lymphocytes. This study evaluated in marrow mononuclear cells (MNCs) of patients with FA, the expression of negative modulators of the hematopoiesis, such as TNF-, IFN-, macrophage inflammatory protein 1 (MIP-1), and surface Fas ligand, and the role of TNF- on FA erythropoiesis in vitro. TNF- and IFN- were significantly overexpressed in stimulated marrow MNCs of FA patients as compared to healthy controls. MIP-1 and Fas ligand were undetectable in patients and controls. In bone marrow cultures, the addition of anti–TNF- increased the size and significantly increased the number of erythroid colony-forming units and erythroid burst-forming units grown from FA patients but not from healthy controls. This indicates that FA subjects have a marrow TNF- activity that inhibits erythropoiesis in vitro. TNF- has a relevant role in the pathogenesis of erythroid failure in FA patients. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? 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