The Stanford researchers now are looking at ways to adapt the technique for use in humans. Those trials would not begin for at least another year, he added. The results of the mouse study were scheduled to be presented Sunday, April 19, by Dr. Richard dal Canto, a graduate student in Fathman's laboratory, at the annual meeting of the Federation of American Societies for Experimental Biology, held in San Francisco. In both diseases, the immune system turns against the very tissues it was designed to protect, attacking a protein called myelin that insulates nerves. The nerve impulses then go awry, causing impaired vision and motor control and leading to a gradual decline in function that ends in death.
Some cytokines suppress inflammation, while others promote it.
To do that, the researchers used specially tailored retroviruses devised by Garry Nolan, a Stanford assistant professor of molecular pharmacology and of microbiology and immunology. Nolan and his colleagues were able to repackage these retroviruses to carry the gene for the suppressor cytokines while disabling the viruses so that they could not reproduce once they were inside the cell. So this is a way of permanently putting the DNA into the cell and getting the cytokine we need to the right part of the body while taking advantage of the homing properties of these immune cells. Dal Canto noted that most treatments for autoimmune diseases, including rheumatoid arthritis and MS, take a global approach, suppressing the immune system generally. But that approach can be dangerous because it leaves the body open to infection, he said.