Growth regulation of the AML-193 leukemic cell line: Evidence for autocrine production of granulocyte-macrophage colony-stimulating factor (GM-CSF), and inhibition of GM-CSF-dependent cell proliferation by interleukin-1 (IL-1) and tumor necrosis factor (tnfα)
✍ Scribed by Vincent Kindler; John Shields; Dominique Ayer; Gonzalo J. Mazzei
- Publisher
- John Wiley and Sons
- Year
- 1991
- Tongue
- French
- Weight
- 583 KB
- Volume
- 47
- Category
- Article
- ISSN
- 0020-7136
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✦ Synopsis
The human leukemic cell line AML-193 was tested for its proliferative response to endogenously produced autocrine factors and to a variety of cytokines and colony-stimulating factors. Cells grown in the absence of GM-CSF incorporated tritiated thymidine, and this was partially reversed by adding neutralizing anti-GM-CSF antibodies to the culture medium, suggesting that it was due, at least in part, to autocrine GM-CSF production. This was confirmed by immunopurification of a GM-CSF-like activity from cell supernatant of AML-193 cells grown in serum free medium in the absence of exogenous GM-CSF. When AML-193 cells were cultured with GM-CSF in combination with other cytokines, Interleukin-I a and fl(1L-1 a and fl), Interleukin-3 (IL-3), Interleukin-6 (IL-6), granulocyte colony-stimulating factor (G-CSF) and tumor necrosis factor a (TNFa), none of them affected the concentration of GM-CSF required to induce 50% of maximum proliferation (D5,,). However, the maximum proliferation induced by GM-CSF alone was drastically decreased by IL-l a, IL-I f3 and TNFa. Inhibition caused by exposure of the AML-193 to IL-l for up to 24 hr was reversible, ruling out a direct cytotoxic effect.