The protective effect of TREM-1 on monocyte survival is mediated by Erk and Akt signaling. Adenovirus expressing TREM-1–infected THP-1 monocytic cells were cultured with 50 mm PD98059 (Erk inhibitor) or 100 nm wortmannin (Akt inhibitor) for 1 h. Then, the cells were added to TREM-1Ab– or phosphate-buffered saline–coated 24-well plate for 24 h, in combination with or without 0.6 μg/ml staurosporine for the last 4 h. Cells were stained with annexin V–fluorescein isothiocyanate/propidium iodide and analyzed by flow cytometry. Results are representative of three independent experiments (A) and data are presented as scatter plots with the mean imposed on the scatter (B). Akt = v-akt murine thymoma viral oncogene homologue; Erk = extracellular signal–regulated kinase; FITC = fluorescein isothiocyanate; PI = propidium iodide; STS = staurosporine; THP-1 = human acute monocytic leukemia cell line; TREM-1Ab = triggering receptor expressed on myeloid cells-1 antibody.