been found in many human tissues and has the capacity to differentiate into tissue-specific cells, including myocytes, hepatocytes, and other cell types114-116. While some studies have reported differences in the prevalence of microchimerism between healthy individuals and patients with autoimmune disease, a more striking difference has often been an increase in the quantity of microchimerism in patients with autoimmune disease110,117-124, including most of the diseases shown in Figure 3c. The idea that the destructive immune response causing disease may be directed at the chimeric cells raised the suggestion that some autoimmune diseases may in fact be alloimmune125. Lastly, the onset of many autoimmune diseases in women during and immediately following the reproductive years has been attributed to microchimerism126, suggesting that exposure to fetal cells during pregnancy is a sex-specific risk factor for autoimmune disease.Box 3. Genetic Imprinting and Parent-of-Origin EffectsOne mechanism for sex-specific transmission of disease or quantitative phenotypes is genomic imprinting, which refers to the transcriptional silencing of a gene in the gamete inherited from either the mother or the father, but not both (i.e., allele-specific silencing). The best studied silencing mechanism is methylation, and differential methylation between alleles is considered the hallmark feature of an imprinted locus127. The
