The researchers found that certain antibodies in female mice attached to an antigen in the cells of their babies. That process then stimulated a response by T-cells, which attacked the ovaries of the baby mice. Eighty to 90 percent of the baby mice had ovarian destruction or inflammation in the study, an indication of autoimmune disease.
Usually, T-cells help direct and control the immune response and are important in the destruction of invaders in the body such as viruses, bacteria and cancer. T-cells also are required for optimum production of antibodies. But under abnormal conditions, the same T-cells can turn on the body's own cells and cause autoimmune disease.
"The findings were unexpected," said Kenneth S. K. Tung, a professor of pathology and microbiology at U.Va. "This suggests that autoimmune disease, in addition to a genetic influence, also has an environmental and non-genetic influence. It is really a new paradigm, a new way of thinking about autoimmune disease."
Tung and his colleagues also found that there is a time window in which exposure to the mother's antibody is critical for development of autoimmune disease. Mice exposed to the maternal antibody did not develop autoimmune disease after the first five days of life. Tung believes that's because special cells that control the action of T cells weren't functioning in the early days of life.
Mice transfer antibodies to their offspring through milk. In humans, the transfer of antibodies from mother to baby happens through the placenta during pregnancy, Tung says.
Autoimmune disease occurs when the normal tolerance of the body to its own cells disappears and healthy cells are attacked. Diabetes mellitus, rheumatoid arthritis, lupus and multiple sclerosis are types of autoimmune disease.
Journal
The Journal of Immunology