A new mathematical model developed by Johns Hopkins researchers offers an explanation of how the body's immune system is triggered into action, which they believe could have long-term applications in the treatment of allergies and other diseases.
The Baltimore team, which worked on it for a decade, suggests a basic "immunon" theory to account for the activation of the defense mechanism, particularly the production of antibodies to fight foreign invaders, from pollen to disease-producing microbes.
The theory proposes that the cells that produce antibodies are turned on only when a "critical" number of one of the areas on their surfaces, known as receptors, cluster together to form "immunons," says Dr. Howard Dintzis, chairman of the department of biophysics at Johns Hopkins School of Medicine.
These surface receptors recognize and chemically attract invading antigens, the foreign substances such as microbes that cause the immune reactions.
The theory is supported by a simple test system involving animals, says Dintzis, but further studies are needed to determine whether it is generally applicable in understanding how the immune system works.
If so, he says that it could be possible, using this approach, to manipulate the immune system--either "enhancing the response" to help fight some diseases, perhaps even cancer, or "turning it down" to make allergic reactions and auto-immune diseases, such as rheumatoid arthritis, less severe.
Dintzis acknowledges, however, that the new research is likely to receive a "skeptical and turbulent response" among researchers studying the immune system. "That's as it should be. It will all come out in the wash," he said.
The research is being published by Dintzis, his wife Renee Dintzis, an assistant professor of cell biology, and Dr. Bert Vogelstein, an assistant professor of oncology, in two papers in the Proceedings of the National Academy of Sciences. It is not yet generally available to the research community.
Some immunologists, who have not yet seen the latest reports but were familiar with preliminary versions, cautioned that the theory appeared to be too simplified to explain what they considered a far more complicated system.
One of them, Dr. Donald Mosier, of the Institute for Cancer Research, said that he felt the Hopkins approach was "incomplete. Even if validated, it wouldn't be a major breakthrough."
But Dr. Manfred Mayer, a Hopkins immunologist who submitted the paper to the prominent journal, was more hopeful. He said that he was "guardedly optimistic" that the new theory would prove a "useful tool. That is why I think it should be published."
He said he was fully aware of the arguments likely to be made against it, but urged his colleagues to "pay a little more attention to this approach," adding that "in scientific research, like everything else, there are fads and fashions. Sometimes good research does not see the light of day."
Mayer said it was "quite possible that this approach may help bring some order" to immunology research. "Often one needs a simple theory in order to design better experiments."
The Hopkins team proposes that immunons are formed by the clustering of about 20 antigen-attracting receptors on the surfaces of special immune system cells called "B" lymphocytes. When enough immunons are formed, they say, the cells begin growing into the mature cells responsible for producing antibodies and fighting the antigens.
Howard Dintzis says the theory would help resolve longstanding "puzzles" in immune reactions, particularly inhibitory effects of very low or very high doses of antigens which would prevent immunons from forming.