RESEARCHERS at The Johns Hopkins Medical Institutions, Baltimore, Md, have used immunoflourescence experiments to elucidate thalidomide's effect on the immune system.
These studies reveal that thalidomide binds less avidly to the helper T lymphocytes than it binds to the suppressor and cytotoxic T lymphocytes— a pattern seen in other immunosuppressive drugs, most notably cyclosporine (Transplant Proc. 1989;21:850-852).
Paradoxically, it is this binding pattern that effectively suppresses the activity of the helper T lymphocytes while allowing for the development of the cytotoxic and suppressor T lymphocytes—cells that play a critical role in keeping graft-versus-host disease (GVHD) in check and allow for transplant tolerance.
Teratogenic Mechanism Puzzling
In terms of adverse effects, however, thalidomide's workings as a teratogen still elude researchers. Two dozen mechanisms, encompassing the biochemical, cellular, and tissue levels, have been proposed (Teratology. 1988; 38:229-239). It is known, however, that the window for embryopathy is small— between days 45 and