InFocus, Vol. 9, No. 1, March 2001
Chance mutations, coupled with a viral infection, can trigger autoimmune reactions that create a potentially deadly situation. The finding, appearing in a recent issue of the Journal of Experimental Medicine, is preliminary and unlikely to produce any help for patients in the near future. However, researchers think that it could one day lead to treatments for lupus, rheumatoid arthritis, and Type 1 diabetes. A prime example of the link is rheumatic heart disease, an autoimmune attack on heart tissue that is thought to result from repeated strep infections during childhood.
Led by Andrew J. Caton, Ph.D., associate professor, Wistar Institute, Philadelphia, the research hinges on a class of immune agents called memory B cells. In the reactions that make up an immune response, the memory B Cells have two key jobs. The first is to recognize an invading organism, such as a virus, and warn other immune cells of its presence. They do this by generating proteins (antibodies) which are specific to the microbe. They can also neutralize the invader by attaching themselves to it.
There is a subset of B cells that, when they meet an invader, choose not to do anything immediately. Rather, they travel to the spleen and, with the help of other immune cells, begin to mutate quickly and randomly. In clusters known as germinal centers, they refine themselves into highly specific cells that flood the bloodstream and defeat the infection. This process, occurring about a week after the initial infection, gives the body a memory of the invader, helping to fight off subsequent attacks from the same organism.
In the latest study of Dr. Caton and his colleagues, it was shown that, during their time in the spleen, these B cells can mutate and become hostile to the individual body. Using a strain of mice genetically modified to express an influenza protein, hemagglutinin, the researchers were able to disguise the viral protein as part of the body. When they infected the previously healthy animals with flu, their immune cells launched a muted attack against the transferred protein. Dr. Caton observes that, since B cells in the first wave of attack die off, the autoimmune reaction had to originate with the B cells produced in the second phase; that is, the combination of random mutations with a viral invasion sparked a mild autoimmune response.
If infections do spark autoimmune reactions, then vaccination would be the obvious answer; yet according to Noel R. Rose, M.D., chair of AARDA National Scientific Advisory Board, at least one other new study seems to show that the incidence of autoimmune disease rises with more immunization. He comments, "That makes life very interesting for people who study these illnesses."
Source: HealthScout Reporter, Dec. 18, 2000
