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)

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Abstract
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, lnterleukin‐1 α and β (IL‐I α and β), lnterleukin‐3 (IL‐3), lnterleukin‐6 (IL‐6), granulocyte colony‐stimulating factor (G‐CSF) and tumor necrosis factor a (TNFα), none of them affected the concentration of GM‐CSF required to induce 50% of maximum proliferation (D50). However, the maximum proliferation induced by GM‐CSF alone was drastically decreased by IL‐I α, IL β and TNFα. Inhibition caused by exposure of the AML‐193 to IL‐I for up to 24 hr was reversible, ruling out a direct cytotoxic effect.

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