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Correlation of interleukin-2 receptor expression with tissue-specific growth of an interleukin-3-dependent autocrine
R Ceredig1, T Robins, H D Campbell
1Department of Medicine and Clinical Science, John Curtin School of Medical Research, Australian National University, Canberra.
An autocrine leukemia (FDC-P1-IL3) has been developed using a retroviral vector containing the interleukin-3 (IL-3) gene to transfect the IL-3-dependent cell line FDC-P1. When leukemia cells were reisolated from experimental animals, it was found that levels of interleukin-2 (IL-2) receptor (IL-2R) expression were greater on cells isolated from the lymph node than on cells isolated from the spleen. Cloned sublines of FDC-P1-IL3 were selected by flow microfluorometry for high or low levels of IL-2R expression. Those clones that expressed high levels of IL-2R grew preferentially in the lymph node. Although IL-2 is not mitogenic for FDC-P1 cells and does not increase the rate of growth of FDC-P1-IL3 cells in vitro, the cloning efficiency of FDC-P1-IL3 is increased fourfold in the presence of IL-2. These observations suggest that the IL-2R on FDC-P1-IL3 cells plays an important role in modulating the growth of this leukemia in sites that contain high levels of IL-2.
An autocrine leukemia (FDC-P1-IL3) has been developed using a retroviral vector containing the interleukin-3 (IL-3) gene to transfect the IL-3-dependent cell line FDC-P1. When leukemia cells were reisolated from experimental animals, it was found that levels of interleukin-2 (IL-2) receptor (IL-2R) expression were greater on cells isolated from the lymph node than on cells isolated from the spleen. Cloned sublines of FDC-P1-IL3 were selected by flow microfluorometry for high or low levels of IL-2R expression. Those clones that expressed high levels of IL-2R grew preferentially in the lymph node. Although IL-2 is not mitogenic for FDC-P1 cells and does not increase the rate of growth of FDC-P1-IL3 cells in vitro, the cloning efficiency of FDC-P1-IL3 is increased fourfold in the presence of IL-2. These observations suggest that the IL-2R on FDC-P1-IL3 cells plays an important role in modulating the growth of this leukemia in sites that contain high levels of IL-2.