IP-10 and MIP-1α inhibit the stimulatory effects of GM-CSF and SLF on ERK2 MAP kinase activity in MO7e cells. Factor-starved MO7e cells were treated with GM-CSF, SLF, or the combination of GM-CSF and SLF (GM + SLF ) for 15 minutes (A) or for various times throughout a 4-hour treatment period (B and C) or were treated with 8-bromo-cAMP (cAMP + GM-CSF + SLF ) (A) or with MIP-1α (MIP-1α + G + S), IP-10 (IP-10 + G + S), PF4 (PF4 + G + S), or IL-8 (IL-8 + G + S) for 1 hour before combined treatment with GM-CSF and SLF for 15 minutes (A) or for various times throughout a 4-hour treatment period (B and C). MAP kinase proteins were immunoprecipitated from cell lysates and the relative kinase activity, as indicated by phosphorylation of the MBP peptide substrate, was determined for each treatment group as described in the Materials and Methods. Control cells received vehicle alone (control, A through C). Values are expressed as the fold increase above control levels. Each bar (A) represents the mean ± the standard deviation of four determinations obtained in separate experiments. Each point (B and C) represents the mean of four determinations obtained in separate experiments. MAP kinase levels for the separate GM-CSF and SLF treatment groups were significantly higher than controls at 15 minutes, 30 minutes, and 1 hour (P < .05). MAP kinase levels for the GM-CSF + SLF group were significantly higher than those for control, GM-CSF, SLF, cAMP + GM-CSF + SLF, MIP-1α + GM-CSF + SLF, and IP-10 + GM-CSF + SLF treatment groups at all time points studied (P < .05) and were significantly higher to a greater-than-additive extent above the combined mean MAP kinase activity for the individual GM-CSF and SLF groups when administered separately (P < .05).