CHARLOTTESVILLE, Va., May 1 In animal studies, researchers at the
University of Virginia Health System have discovered a new mechanism that may
trigger autoimmune disease in newborn babies. The research is published in the
May issue of the Journal of Immunology.
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.
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