MECHANISM OF DIFFERENTIATING ACTION OF L-GLUTAMIC ACID ON HL-60 CELLS

To elucidate the mechanism whereby L-glutamic acid (L-Glu) causes HL-6 0 cells to differentiate via the granulocyte pathway, we examined the reception by these cells of recombinant human interleukin 1 beta (rHuI L-1 beta>, tumor necrosis factor alpha (rHuTNF-alpha), interferon gamm a (rHuIFN-gamma), IL-6 (rHuIL-6), and IL-2 (rHuIL-2). The high-affinit y binding of [I-125]rHuIL-1 beta (K-d = 0.32 nM), [I-125]rHuIFN-gamma (K-d = 0.28 nM), and [I-125]rHuIL-6 (K-d = 0.075 nM) became low-affine in the presence of 0.1 mu M L-Glu (respectively 13.3, 10.0, and 2.1 n M). At d the same time, 1-h incubation of HL-60 cells with 0.1 mu M L- Glu increased 2.4-fold the number of high-affinity binding sites for [ I-125]rHuTNF-alpha and had no effect on the reception of [I-125]rHuIL- 2.