Persistence of maternal and fetal cells in autoimmune diseases

Abstract

It has long been known that maternal proteins are transported to the fetus during pregnancy. Maternal antibodies provide immunity for the newborn infant during the first six months of life. Only recently with the advent of ultrasensitive DNA detection techniques has it been established that there is bidirectional traffic of not only antibodies but also cells. The term “chimerism” is used when one individual harbors cells from another individual; “microchimerism” refers to low levels of chimerism. When cells traffic between fetus and mother during pregnancy and persist, maternal and fetal microchimerism results. Chronic graft-versus-host disease (GVHD) is a condition of chimerism that shares clinical characteristics with some autoimmune diseases. Human leukocyte antigen (HLA) class II genes are known to be important both in autoimmune disease and in GVHD. When considered together, these observations led to the hypothesis that microchimerism and HLA genes of host and nonhost cells are involved in autoimmune disease. Sources of nonhost cells include cells transferred during pregnancy (maternal and fetal), a twin or unrecognized lost twin, or a blood transfusion. By this hypothesis, women who have been pregnant have an increased risk of autoimmune disease because they have two sources of microchimerism: maternal and fetal. Studies of systemic sclerosis, primary biliary cirrhosis, Sjogren’s syndrome, pruritic eruption of pregnancy, myositis, neonatal lupus, and thyroid disease have both lent support and raised doubts about the role of microchimerism in autoimmune disease.