The modulation of soluble CD16 titers in human immunodeficiency virus (HIV)-infected patients' serum, with an initial increase in Centers for Disease Control (CDC) clinical stage II and III patients followed by a dramatic drop in patients with AIDS (CDC clinical stage IV), is reported. These changes are statistically correlated with the CDC staging system, the number of CD4+ cells, the amount of p24 antigen in serum, and the anti-p24 antibody titers, indicating the potential value of soluble CD16 titer as an easily available serum marker of disease progression. To evaluate a possible link between this observation and the expression of membrane-associated CD16/FcRIII, flow cytometry immunofluorescence analysis was performed on peripheral blood lymphocytes from patients in three CDC stages; no specific changes in the number of natural killer cells expressing CD16+ antigens or in the total number of Leu19+ cells were found. However, there was a statistical correlation between the absolute number of T cells expressing CD16 antigens (CD3+/CD16+) and the modulated titers of soluble CD16 in HIV-infected serum.
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.
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