Selective generation of erythroid burst-promoting activity by recombinant
interleukin 2-stimulated human T lymphocytes and natural killer cells
S Skettino, J Phillips, L Lanier, A Nagler and P Greenberg
Department of Medicine, Stanford University Medical Center, Palo Alto, CA.
Because T lymphocytes and natural killer (NK) cells produce a variety of
growth factors and interleukin 2 (IL2) modulates the activity of both, we
assessed the ability of IL2 to stimulate human T cells and NK cells to
produce hematopoietic growth factors detectable in clonogenic marrow
culture. Human recombinant interleukin 2 (rIL2) added directly to cultures
of human bone marrow that had been depleted of monocytes or depleted of
both monocytes and T cells caused no significant alteration of myeloid
(CFU-GM) or erythroid colony formation. Conditioned media harvested from
rIL2-stimulated (greater than 100 U/mL) peripheral blood mononuclear cells,
T cells, Leu-2 cells, and Leu-3 cells all had erythroid burst-promoting
activity (BPA) but lacked myeloid colony- stimulating factor (GM-CSF) or
CFU-GM-inhibitory activity. These T cells were IL2 receptor-negative, and
the addition of anti-IL2 receptor monoclonal antibody (anti-Tac) to T cell
cultures did not abrogate this IL2-stimulated BPA production. In addition,
Percoll gradient-enriched, large granular lymphocytes (LGL) were separated
by fluorescence- activated cell sorting into Leu-11+ (NK) cells and Leu-11-
(low-density Leu-4+ T) cell fractions. rIL2 stimulated LGL, Leu-11+ and
Leu-11- cells to produce BPA but not detectable GM-CSF or CFU-GM-inhibitory
activity. Leu-11+ (NK) cells were Tac-negative from days 0 through 14 of
culture. We conclude that rIL2 at high concentrations stimulated T cells,
Leu-2 and Leu-3 cell subsets, LGL, and NK cells to produce BPA but not
GM-CSF and that this stimulation may be mediated by an IL2 receptor
distinct from Tac or by an epitope of the IL2 receptor not recognized by
the anti-Tac antibody.
Volume 71,
Issue 4,
pp. 907-914,
04/01/1988
Copyright © 1988 by The American Society of Hematology
