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Division of Research Immunology/Bone Marrow Transplantation, Childrens Hospital Los Angeles, Los Angeles, CA 90027
The effect of IL-3 on the B lymphoid potential of human hemopoietic
stem cells is controversial. Murine studies suggest that B cell
differentiation from uncommitted progenitors is completely prevented
after short-term exposure to IL-3. We studied B lymphopoiesis after
IL-3 stimulation of uncommitted human
CD34+CD38- cells, using the stromal cell line
S17 to assay the B lymphoid potential of stimulated cells. In contrast
to the murine studies, production of CD19+ B cells from
human CD34+CD38- cells was significantly
increased by a 3-day exposure to IL-3 (p < 0.001).
IL-3, however, did not increase B lymphopoiesis from more mature
progenitors (CD34+CD38+ cells) or from
committed CD34-CD19+ B cells. B cell
production was increased whether CD34+CD38-
cells were stimulated with IL-3 during cocultivation on S17 stroma, on
fibronectin, or in suspension. IL-3R
expression was studied in
CD34+ populations by RT-PCR and FACS. High IL-3R protein
expression was largely restricted to myeloid progenitors.
CD34+CD38- cells had low to undetectable
levels of IL-3R by FACS. IL-3-responsive B lymphopoiesis was
specifically found in CD34+ cells with low or undetectable
IL-3R protein expression. IL-3 acted directly on progenitor cells;
single cell analysis showed that short-term exposure of
CD34+CD38- cells to IL-3 increased the
subsequent cloning efficiency of B lymphoid and B lymphomyeloid
progenitors. We conclude that short-term exposure to IL-3 significantly
increases human B cell production by inducing proliferation and/or
maintaining the survival of primitive human progenitors with B lymphoid
potential.
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