Mechanism of differentiating action of L-glutamic acid on HL-60 cells

To elucidate the mechanism whereby L-glutamic acid (L-Glu) causes HL-60 cells to differentiate via the granulocyte pathway, we examined the reception by these cells of recombinant human interkukin 1β (rHuIL-1β), tumor necrosis factor α (rHuTNF-α), interferon γ (rHuIFN-γ), IL-6 (rHuIL-6), and IL-2 (rHuIL-2). The high-affinity binding of [¹²⁵I]rHuIL-1β (K_d = 0.32 nM), [¹²⁵I]rHuIFN-γ (K_d = 0.28 nM), and [¹²⁵I]rHuIL-6 (K_d = 0.075 nM) became low-affine in the presence of 0.1 μM L-Glu (respectively 13.3, 10.0, and 2.1 nM). At the same time, 1-h incubation of HL-60 cells with 0.1 μM L-Glu increased 2.4-fold the number of high-affinity binding sites for [¹²⁵I]rHuTNF-α and had no effect on the reception of [¹²⁵I]rHuIL-2.