The application of molecular biological techniques to the study of human pregnancy has resulted in the recognition of bidirectional cell traffic at the fetal-maternal interface. Fetal progenitor cells have been found to persist in the maternal peripheral blood for decades after childbirth. Scleroderma has a strong predilection for women, a peak incidence in women following childbearing years, and clinical similarities to chronic graft-versus-host disease that occurs after allogeneic stem cell transplantation. This article explores the hypothesis that microchimerism contributes to the pathogenesis of scleroderma and reviews early studies that lend support to this hypothesis. Chimerism is used to indicate a body that contains cell populations derived from different individuals; microchimerism indicates low levels of chimerism. A mechanism by which microchimerism might contribute to the pathogenesis of scleroderma is unknown, but insights can be gained through knowledge garnered in studies of microchimerism in transplantation biology. Although high-lighted in the study of scleroderma, microchimerism is also implicated in selected other autoimmune disorders.