FcγRIIIa (CD16) Induction on Human T Lymphocytes and CD16pos T-Lymphocyte Amplification

During serial assays designed to amplify natural killer (NK) cells in vitro, we observed that when peripheral blood mononuclear cells (PBMCs) from human immunodeficiency virus positive (HIV +) patients were stimulated for 2 weeks with an Epstein-Barr virus-infected B lymphoblastic cell line and interleukin-2, a well known procedure to amplify NK cells in vitro, 44.4 +/- 18% CD3(+)CD16(pos) T lymphocytes were recovered together with NK cells, of which 78.2% expressed an alpha beta T-cell receptor (TCR). To identify the T-cell compartment from which they originated (naive, antigen experienced, CD16(pos), or CD16(neg)), we first compared the results obtained with HIV + patients' PBMCs (where essentially all CD8 cells are antigen experienced) with those obtained from cord blood lymphocytes (essentially naive) and PBMC from healthy donors (with variable antigen experience). Two weeks after stimulation, alpha beta TCR CD16(pos) T lymphocytes increased from 0.3%, 2.2%, and 8.2% to 2.5%, 7.7%, and 36.3%, for cord blood, healthy donors, and HIV + patients, respectively. Second, using cell-sorting experiments for CD16(neg) cells and antibody-dependent cellular cytotoxicity assays, we demonstrated that a functional CD16 receptor could also be induced at the cell surface of alpha beta TCR CD16(pos) T lymphocytes. Together, these results demonstrate that under stimulation conditions known to induce NK cell proliferation, a subset of alpha beta TCR CD16(pos) T cells arises from antigen-experienced CD16(pos) cells but also from antigen-experienced CD16(neg) T lymphocytes, revealing the possibility to increase a patient's antibody-dependent cellular cytotoxicity potential through simple stimulation of this particular memory compartment.