Because thalidomide does not kill the leprosy bacteria directly, scientists believe that it probably modulates the immune system's response to the bacteria, thus reducing the dermatological symptoms of ENL even though the bacteria may still be present. Scientists have attempted to exploit thalidomide's effects on the immune system to their advantage. For example, many diseases, such as rheumatoid arthritis and lupus, are due to autoimmunity, which means that a person's immune system somehow fails to recognize his own tissues, and the immune system attacks them. Researchers have used thalidomide as an investigational drug on several dermatological conditions in cases that did not respond to standard therapies, including ENL, prurigo nodularis, actinic prurigo, and discoid lupus erythematosus. All these studies were done under strict monitoring of the patients' clinical symptoms, side effects, and perhaps most importantly, pregnancy status.
Active research is underway to see what other diseases can be targeted.
Despite clinical evidence that thalidomide somehow modulates the immune system, its mode of action is not clear, nor is its target in the immune system. Undoubtedly the answer is complex. Thalidomide has also been shown to inhibit angiogenesis, the process by which new vessels reach out to supply growing tissues with blood. This may be the main reason thalidomide causes birth defects. Without normal angiogenesis in the developing fetus, the arms and legs, as well as internal organs, cannot develop properly.