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Biologic response to anti-CD16 monoclonal antibody therapy in a human
immunodeficiency virus-related immune thrombocytopenic purpura patient
C Soubrane, JM Tourani, JM Andrieu, S Visonneau, K Beldjord, D Israel-Biet, R Mouawad, J Bussel, M Weil and D Khayat
Medical Oncology Laboratory, Salpetriere Hospital, Paris, France.
A patient with refractory human immunodeficiency virus (HIV)-related immune
thrombocytopenic purpura (ITP) was treated with 3G8 (anti-CD16) monoclonal
antibody on days 1, 3, and 8 (25, 25, and 50 mg were administered
intravenously, respectively). Side effects were those expected after the
administration of a xenogenic protein, but a severe bone pain occurred from
the second injection. At the time of the initiation of the treatment the
platelet count was 20,000/mm3 and the absolute CD4 number was 100/mm3. We
obtained a long-term correction of thrombocytopenia and, to a lesser
extent, there was a stabilization of CD4 lymphocytes for 18 months. We
observed a significant stimulation of natural killer (NK) function and an
elevation in the serum level of tumor necrosis factor alpha, interferon
gamma, and granulocyte- macrophage colony-stimulating factor. This suggests
that in HIV-related ITP the removal of platelets is mediated by
low-affinity Fc gamma receptors (CD16). The stimulation of NK function and
elevation in CD4+ lymphocytes may be related to the production of cytokines
by activated human NK cells through the interaction of their CD16-bearing
receptor with the 3G8 monoclonal antibody. This observation warrants
confirmation and further clinical trials.
Volume 81,
Issue 1,
pp. 15-19,
01/01/1993
Copyright © 1993 by The American Society of Hematology
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