S. BLANCHE, M.D.; F. Le DEIST, M.D.; F. VEBER, M.D.; G. LENOIR, M.D.; A.M. FISCHER, M.D.; J. BROCHIER, Ph.D.; C. BOUCHEIX, Ph.D.; M. DELAAGE, M.D.; C. GRISCELLI, M.D.; A. FISCHER, M.D.
We treated two children who developed Epstein-Barr virus-induced polyclonal B-cell proliferation after HLA-mismatched bone marrow transplantation for congenital immunodeficiency with two monoclonal anti-B-cell antibodies. Lymphoproliferative syndrome occurred between 50 and 60 days after bone marrow infusion, and was diagnosed by the presence of spontaneously growing B cells containing Epstein-Barr nuclear antigen in the blood and bone marrow. The mouse monoclonal anti-B-cell antibodies used were a CD21-specific antibody recognizing the CR2 receptor on B cells (BL13, lgG1) and a CD24-specific antibody binding B cells at all steps of differentiation (ALB9 lgG1). Both antibodies were given intravenously (0.2 mg/kg/body weight · d for 10 days). All clinical and biological manifestations resolved within 3 weeks of treatment. Recurrence was not seen at 18- and 15-month follow-ups. T-cell function developed normally; B-cell function remained partially deficient in one patient 21 months after bone marrow transplantation. These results suggest that monoclonal anti-B-cell antibodies could be useful in controlling severe polyclonal lymphoproliferative syndrome in profoundly immunodeficient patients after bone marrow transplantation.
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BLANCHE S, Le DEIST F, VEBER F, LENOIR G, FISCHER A, BROCHIER J, et al. Treatment of Severe Epstein-Barr Virus-Induced Polyclonal B-Lymphocyte Proliferation by Anti-B-Cell Monoclonal Antibodies: Two Cases After HLA-Mismatched Bone Marrow Transplantation. Ann Intern Med. 1988;108:199–203. doi: 10.7326/0003-4819-108-2-199
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Published: Ann Intern Med. 1988;108(2):199-203.
Hematology/Oncology, Infectious Disease.
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Print ISSN: 0003-4819 | Online ISSN: 1539-3704
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