A research team which included several Medical School faculty members reported last week that they had isolated a key immune system protein which may lead to drugs designed to prevent organ transplant rejections.

Such rejection occurs when the recipient's immune system recognizes the organ as foreign, and "killer" T cells begin attacking the cells which compose it.

Led by assistant professor of pathology Anjana Rao, the team reported in Science that they had discovered genes which code for NFATp, a protein involved in stimulating the creation of new T cells.

Until now, the drug cyclosporin has prevented organ transplant rejection by blocking an enzyme involved in the creation of T cells. But extended treatment with cyclosporin leads to toxicity and suppresses the immune response, leaving a patient vulnerable to other diseases, according to Rao.

With the gene sequence of NFATp, "we may be able to create a drug specific to NFAT without the harmful effects of cyclosporin," said Rao.

Other collaborators on the paper include Gregory L. Verdine, professor of chemistry, and Patrick G. Hogan, lecturer on neurobiology at Harvard Medical School.