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. 2003 Mar 17;197(6):763–775. doi: 10.1084/jem.20020150

Figure 2.

Figure 2.

Proliferation induced by rIL-15 and rGM-CSF: IL-15R/GM-CSFR cross talk in TF1β cells. (A) Proliferative response of TF1β cells to recombinant IL-15 and GM-CSF. TF1β (IL-15Rα/β/γc) CD34+ cells were cultured for 4 d with rIL-15 or rGM-CSF (10 ng/ml) and their proliferation potential was then analyzed. Sister cultures were continuously incubated with neutralizing mAbs recognizing the IL-15Rα, γc, and GM-CSFRβ chains. In TF1β cells cultured with rIL-15, the proliferation rates of samples treated with an anti–GM-CSFRβ mAb were significantly higher (+25%; P < 0.001) than those of samples incubated with rIL-15 alone or with rIL-15 plus an anti-γc mAb. (B) Proliferative response of Raji cells to rIL-15. Raji cells (IL-15Rα/γc) were cultured for 4 d with rIL-15 (10 ng/ml) and analyzed for proliferation. Sister cultures were continuously incubated with neutralizing mAbs recognizing the IL-15Rα, γc, and GM-CSFRβ chains. (C) Proliferative response of TF1β cells to MS9 cells. TF1β cells were cocultured for 4 d with MS9 cells and analyzed for proliferation. Sister cultures were continuously incubated with neutralizing mAbs recognizing the GM-CSFRα, GM-CSFRβ, IL-15Rβ/γc, IL-15Rα chains, and IL-15. Cells were counted in an electronic Coulter counter and the data are expressed as % difference in proliferative potential with respect to control untreated samples. The data presented are representative of three independent experiments.