Thalidomide causes congenital anomalies and it is immunomodulatory. Th
ese properties could be explained by an ability to alter the orderly p
rocess of programmed cell death during embryogenesis and modulation of
apoptosis of lymphoid and/or myeloid cells in the immune response. Ap
optosis of lymphoid and myeloid cells was studied by measuring the per
centage of cells capable of excluding propidium iodide and expressing
phosphatidylserine on their outer membrane. In addition, expression of
Fc gamma RIII (CD 16) was used to assess neutrophil apoptosis. Thalid
omide did not affect the rate of apoptosis of CTLL-2 cells deprived of
, or supplemented with, IL-2; of T-cells (mitogen-stimulated or restin
g) or of neutrophils. However, neutrophils obtained from HIV-infected
patients treated with thalidomide showed reduced expression of CD16, a
surrogate marker for apoptosis of neutrophils. Thalidomide's effect o
n neutrophil apoptosis in vivo warrants further investigation.