exist after blood transfusions to a severely immunocompromised population of patients who suffered trauma. Other possible sources of microchimerism include gestation, an individual's older sibling, twin sibling, or vanished twin, with the cells being received in utero. Fetal-maternal microchimerism is especially prevalent after abortion or miscarriage. Animal Microchimerism occurs in most pairs of twins in cattle. In cattle (and other bovines), the placentas of fraternal twins usually fuse and the twins share blood circulation, resulting in exchange of cell lines. If the twins are a male–female pair, then XX/XY microchimerism results, and male hormones partially masculinize the heifer (female), creating a martin heifer or freemartin. Freemartins appear female, but are infertile and so cannot be used for breeding or dairy production. Microchimerism provides a method of diagnosing the condition, because male genetic material can be detected in a blood sample. Fetomaternal microchimerism in the brain Several studies have identified male DNA in both the human and mouse brains of mothers following pregnancy with a male fetus. It has been suggested that the fetal-derived cells can differentiate into those capable of presenting neurotypical immunomarkers on their surface. There has been no strong evidence to say microchimerism of the maternal brain leads to disease, however, Parkinson’s disease correlates with a higher incidence of brain microchimeras. Alzheimer’s disease studies support nearly the opposite correlation, the more fetal-derived cells present, the lower the chance of the patient having had Alzheimer’s. Maternal tolerance to paternal-fetal antigens There are many mechanisms at the maternal-fetal interface to prevent immune rejection of fetal cells. Nevertheless, systemic immunological changes occur in pregnant women. For example, condition of women suffering from autoimmune disorders (e.g. rheumatoid arthritis, multiple sclerosis) improves during pregnancy. These changes in immune responses during pregnancy extend to maternal components specific to fetal antigens, because of feto-maternal cell transfer and their retention in mother tissues. During pregnancy, numbers of fetal cells in maternal tissues increase and correlate with expansion of CD4+ regulatory T cells (Tregs). Decreased expansion and decidual accumulation of Treg cause pregnancy complications (preeclampsia, abortions). In mice models, most mother’s fetal-specific CD8+ T cells undergo clonal deletion and express low levels of chemokine receptors and ligands – this prevents remaining fetal-specific CD8+ T cells from entering the maternal-fetal interface. Mother’s fetal-specific CD4+ T cells proliferate, and due to FOXP3 expression, differentiate into Treg cells. Mice models show that fetal-specific Treg cells are necessary for successful pregnancy.