Effect of thalidomide on apoptosis of lymphocytes and neutrophils

Thalidomide causes congenital anomalies and it is immunomodulatory. These properties could be explained by an ability to alter the orderly process of programmed cell death during embryogenesis and modulation of apoptosis of lymphoid and/or myeloid cells in the immune response. Apoptosis of lymphoid and myeloid cells was studied by measuring the percentage 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. Thalidomide did not affect the rate of apoptosis of CTLL-2 cells deprived of, or supplemented with, IL-2; of T-cells (mitogen-stimulated or resting) 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 on neutrophil apoptosis in vivo warrants further investigation.