GM-CSF bioactivity is severely reduced in the lungs of iPAP patients. (A) Bioassay used to quantify GM-CSF bioactivity in BALF. TF-1 cells survived and proliferated in a dose-dependent fashion in the presence of GM-CSF added to the culture medium. Each point represents the mean of 6 determinations. (B) Quantification of inhibition of GM-CSF bioactivity by BALF of iPAP patients. Addition of 20% (vol/vol) BALF from healthy control subjects (closed symbols, n = 6 per point) or iPAP patients (open circles, n = 8 per point). Compared with cells cultured with medium without BALF (as in panel A), adding BALF from healthy controls had no measurable effect on the GM-CSF-dependent survival of TF-1 cells. In contrast, iPAP-BALF significantly inhibited GM-CSF-dependent survival of TF-1 cells (^**P < .002 or ^*P < .05). This inhibitory effect was overcome by the addition of large amounts of GM-CSF to the medium. (C) Deficit of pulmonary GM-CSF bioactivity in iPAP. The bioactivity of GM-CSF in BALF from healthy controls or iPAP patients was calculated as described in “Patients, materials, and methods” and was shown as aggregate data in panel B. The deficit in GM-CSF bioactivity is expressed in nanogram of GM-CSF per milliliter of BALF. Error bars indicate SD.